Journal articles on the topic 'Atropine Physiological effect'
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1
Kang, Seyoon, Yun Jeong Chae, Sun Kyung Park, Taek Geun Kim, and Han Bum Joe. "Prevention of Bradycardia during Spinal Anesthesia under Dexmedetomidine Sedation in Older Adults." Journal of Clinical Medicine 11, no. 21 (October 27, 2022): 6349. http://dx.doi.org/10.3390/jcm11216349.
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Older adults exhibit reduced physiological responses to beta-adrenergic stimulation and parasympathetic inhibition. This study aimed to investigate the effect of reducing the incidence of bradycardia in the atropine and ephedrine pretreatment group compared to the control group in older adults who received spinal anesthesia with intravenous dexmedetomidine. Overall, 102 older adults aged over 65 years were randomly divided into three groups, and saline (control group), atropine at 0.5 mg (atropine group), and ephedrine at 8 mg (ephedrine group) were administered intravenously to each group as pretreatment. Immediately after spinal anesthesia, dexmedetomidine loading and study drug injections were commenced. The primary outcome was the incidence of bradycardia (<50 beats per min) within 60 min following dexmedetomidine loading. The incidence of bradycardia requiring atropine treatment was significantly higher in the control group than in the atropine and ephedrine groups (27.3% vs. 6.1% and 8.8%, respectively; p = 0.035), and no difference was noted between the atropine and ephedrine groups. Therefore, if ephedrine or atropine is selected and used according to the patient’s condition and clinical situation, it may be helpful in preventing bradycardia during spinal anesthesia using dexmedetomidine in older patients.
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Silva, Luiz Eduardo Virgilio, Carlos Alberto Aguiar Silva, Helio Cesar Salgado, and Rubens Fazan. "The role of sympathetic and vagal cardiac control on complexity of heart rate dynamics." American Journal of Physiology-Heart and Circulatory Physiology 312, no. 3 (March 1, 2017): H469—H477. http://dx.doi.org/10.1152/ajpheart.00507.2016.
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Analysis of heart rate variability (HRV) by nonlinear approaches has been gaining interest due to their ability to extract additional information from heart rate (HR) dynamics that are not detectable by traditional approaches. Nevertheless, the physiological interpretation of nonlinear approaches remains unclear. Therefore, we propose long-term (60 min) protocols involving selective blockade of cardiac autonomic receptors to investigate the contribution of sympathetic and parasympathetic function upon nonlinear dynamics of HRV. Conscious male Wistar rats had their electrocardiogram (ECG) recorded under three distinct conditions: basal, selective (atenolol or atropine), or combined (atenolol plus atropine) pharmacological blockade of autonomic muscarinic or β1-adrenergic receptors. Time series of RR interval were assessed by multiscale entropy (MSE) and detrended fluctuation analysis (DFA). Entropy over short (1 to 5, MSE1–5) and long (6 to 30, MSE6–30) time scales was computed, as well as DFA scaling exponents at short (αshort, 5 ≤ n ≤ 15), mid (αmid, 30 ≤ n ≤ 200), and long (αlong, 200 ≤ n ≤ 1,700) window sizes. The results show that MSE1–5 is reduced under atropine blockade and MSE6–30 is reduced under atropine, atenolol, or combined blockade. In addition, while atropine expressed its maximal effect at scale six, the effect of atenolol on MSE increased with scale. For DFA, αshort decreased during atenolol blockade, while the αmid increased under atropine blockade. Double blockade decreased αshort and increased αlong. Results with surrogate data show that the dynamics during combined blockade is not random. In summary, sympathetic and vagal control differently affect entropy (MSE) and fractal properties (DFA) of HRV. These findings are important to guide future studies. NEW & NOTEWORTHY Although multiscale entropy (MSE) and detrended fluctuation analysis (DFA) are recognizably useful prognostic/diagnostic methods, their physiological interpretation remains unclear. The present study clarifies the effect of the cardiac autonomic control on MSE and DFA, assessed during long periods (1 h). These findings are important to help the interpretation of future studies.
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Klongsiriwet, Chaweewan, Janyaporn Wungpanya, Hanafarah Salaemae, Suchanan Thavonsuk, and Siriphun Hiranyachattada. "Physiological Effects of Condensed Tannins from Black Currant (Ribes nigrum L.) on Isolated Rat Duodenal Contraction." Trends in Sciences 19, no. 20 (October 11, 2022): 6233. http://dx.doi.org/10.48048/tis.2022.6233.
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Condensed tannins (CTs) extracted from various plants have been shown to possess antioxidant, antidiabetic, anthelmintic, anti-palatable and anti-diarrhea activity. Black currant (Ribes nigrum L.), a native plant of northern Europe and Asia, is rich in phenolic compounds, including CTs. Among the biological activities of CTs, their astringent property is likely to affect gastrointestinal motility. This study aimed to investigate the physiological effect of CTs from black currant (R. nigrum L.) leaves on isolated rat duodenal contraction. Duodenal segments were fixed in organ baths containing carbogen aerated Krebs solution at the resting tension of 0.7 - 0.8 g. The frequency, amplitude, and tone of duodenal contraction were recorded. Either CTs or acetylcholine (ACh) were cumulatively added into the bath at the concentration of between 0.001 - 10 µg/mL and 10–8 - 10–4 M, respectively. The mechanisms of CTs and ACh actions were studied using muscarinic receptor antagonist (atropine, 1.55×10–5 M) and calcium channel blocker (verapamil, 10–6 M). It is found that CTs at the concentration between 0.001 - 10 µg/mL had no direct effect on duodenal frequency, amplitude, and tone of contraction, whereas ACh showed a significant increase in tonic contraction, was suppressed by atropine. Interestingly, in the presence of atropine and verapamil, CTs showed a further significant decrease in the amplitude of duodenal contraction compared to the effect of these 2 blockers alone. It is concluded that CTs would synergize the activity of the muscarinic receptor antagonist and the calcium channel blocker at duodenal enteric neurons or smooth muscle membrane. However, the use of CTs from black currant (R. nigrum L.) leaves to treat gastro-intestinal disorders while having muscarinic receptor antagonist or calcium channel blocker need cautions.
HIGHLIGHTS
Black currant (Ribes nigrum L.), a native plant of northern Europe and Asia, is rich in phenolic compounds including condensed tannins (CTs) and their astringent property is likely to affect gastrointestinal motility
CTs isolated from leaves of black currant (R. nigrum L.) at the physiological doses (0.001 - 10.0 µg/mL) have no direct effect on isolated rat duodenal contraction
CTs may possess the synergistic or additive effect with either atropine, a nonselective muscarinic receptor, or verapamil, a calcium channel blocker on duodenal amplitude of contraction
GRAPHICAL ABSTRACT
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Paterson, W. G., T. T. Hynna-Liepert, and M. Selucky. "Comparison of primary and secondary esophageal peristalsis in humans: effect of atropine." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 1 (January 1, 1991): G52—G57. http://dx.doi.org/10.1152/ajpgi.1991.260.1.g52.
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To determine whether physiological differences exist between primary (swallow-induced) and secondary (distension-induced) peristalsis in humans, 10 healthy male volunteers underwent esophageal manometry on 2 consecutive days using a perfused intraluminal catheter system that incorporated a latex balloon. Initially the catheter was positioned so that the balloon was centered 16 cm above the lower esophageal sphincter (LES), and intraluminal pressures were recorded 21, 11, 6, and 1 cm above the LES. After a series of wet swallows, dry swallows, and balloon distensions, the catheter was repositioned so that the balloon was 6 cm above the LES and pressures were recorded 1 and 11 cm above the LES. A series of balloon distensions were repeated in this position, and the subject was then given either atropine (10 micrograms/kg iv) or placebo in a double-blind randomized fashion (on consecutive days). The protocol was then repeated in reverse order. Distension-induced responses aboral to the balloon with the balloon located 16 cm above the LES were 1) of lower amplitude, 2) more often nonperistaltic, and 3) less atropine sensitive than swallow-induced contractions at comparable sites. With the balloon located distally (6 cm above LES) contractions induced at the 11-cm site (i.e., orad to the balloon) were much more atropine sensitive than contractions induced at the same site when the balloon was located proximally (i.e., 16 cm above LES). These data suggest that, contrary to previous reports, secondary peristalsis differs significantly from primary peristalsis. Furthermore, atropine differentially effects these two types of peristalsis, suggesting that the neural pathways involved are dissimilar.
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Armstrong, R. B., and M. H. Laughlin. "Atropine: no effect on exercise muscle hyperemia in conscious rats." Journal of Applied Physiology 61, no. 2 (August 1, 1986): 679–82. http://dx.doi.org/10.1152/jappl.1986.61.2.679.
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The purpose of this study was to test the hypothesis that muscarinic cholinergic receptors are involved in the initial vasodilation in red muscle vascular beds of conscious rats performing slow locomotory exercise. Atropine sulfate (1 mg/kg, ia) was administered to one group of rats in which distribution of cardiac output was estimated with radiolabeled microspheres immediately before exercise while the animals were standing on the treadmill and at 30 s and 5 min of treadmill walking at 15 m/min. Blood flows within and among muscles in the atropine-treated animals were compared with flows in control rats that were given a sham injection of an equal volume of physiological saline. Heart rates were elevated above those of control animals in the atropinized rats during preexercise (+17%) and at 30 s of exercise (+15%). However, distributions and magnitudes of blood flows in nonmuscular tissues and within and among skeletal muscles were the same (P greater than 0.05) in atropinized and control rats during preexercise and at both exercise times, indicating that atropine had no effect on the distribution of cardiac output in the rats. It is concluded that muscarinic cholinergic receptors do not play a significant role in elevating muscle blood flow in conscious rats, either during the preexercise anticipatory phase or during slow locomotory exercise.
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Jo, Y. H., Y. L. Lee, K. Y. Lee, T. M. Chang, and W. Y. Chey. "Neurohormonal mechanism of pancreatic exocrine secretion stimulated by sodium oleate and L-tryptophan in dogs." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 1 (July 1, 1992): G12—G16. http://dx.doi.org/10.1152/ajpgi.1992.263.1.g12.
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In the present investigation, we have studied the effect of atropine on the pancreatic secretion stimulated by intraduodenal administration of either sodium oleate or exogenous cholecystokinin (CCK). In four dogs prepared with gastric and Thomas duodenal cannulas, pancreatic juice was collected for measurement of volume, bicarbonate, and protein output, and peripheral venous blood samples were obtained for radioimmunoassay of both secretin and CCK. Volume, bicarbonate, and protein output of the pancreatic juice increased significantly in response to sodium oleate (1-4 mmol/h) in a dose-dependent manner. The increase in pancreatic secretion paralleled the increments in both plasma CCK and secretin. Atropine given intravenously suppressed completely both pancreatic secretion and release of CCK stimulated by sodium oleate, whereas the release of secretin was not affected. Pancreatic secretion was significantly increased in a dose-dependent manner by exogenous CCK octapeptide (CCK-8) at 16, 32, and 64 micrograms (14, 28, and 56 pmol).kg-1.h-1. Atropine inhibited protein output only partially, but it did not influence bicarbonate output. In five additional dogs, the effect of atropine on L-tryptophan-stimulated pancreatic secretion was studied. Interestingly, atropine failed to influence the CCK release and pancreatic secretion of volume and bicarbonate, except for protein secretion, which was significantly inhibited. It was shown previously that atropine inhibited significantly the pancreatic secretion of bicarbonate stimulated by secretin in physiological doses. Thus we conclude that the inhibition by atropine of the pancreatic exocrine secretion stimulated by sodium oleate is mediated by both suppression of CCK release and inhibition of action of secretin on the exocrine pancreas.(ABSTRACT TRUNCATED AT 250 WORDS)
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Zhang, Xiang-Yang, N. Edward Robinson, and Feng-Xia Zhu. "Modulation of ACh release from airway cholinergic nerves in horses with recurrent airway obstruction." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 5 (May 1, 1999): L769—L775. http://dx.doi.org/10.1152/ajplung.1999.276.5.l769.
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To evaluate the functional status of neuronal α2-adrenoceptors (ARs) and β2-ARs on ACh release in horses with recurrent airway obstruction (RAO), we examined the effects of the physiological agonists epinephrine (Epi) and norepinephrine (NE) and the β2-agonists RR- and RR/ SS-formoterol on ACh release from airway cholinergic nerves of horses with RAO. Because SS-formoterol, a distomer of the β2-agonist, increases ACh release from airways of control horses only after the autoinhibitory muscarinic receptors are blocked by atropine, we also tested the hypothesis that if there is an M2-receptor dysfunction in equine RAO, SS-formoterol should increase ACh release even in the absence of atropine. ACh release was evoked by electrical field stimulation and measured by HPLC. Epi and NE caused less inhibition of ACh release in horses with RAO than in control horses. At the catecholamine concentration achieved during exercise (10−7 M), the inhibition induced by Epi and NE was 10.8 ± 13.2 and 3.4 ± 6.8%, respectively, in equine RAO versus 41.0 ± 6.4 and 27.1 ± 5.6%, respectively, in control horses. RR- and RR/ SS-formoterol (10−8 to 10−5 M) increased ACh release to a similar magnitude as that in control horses. These results indicate that neuronal β2-ARs are functioning; however, the α2-ARs are dysfunctional in the airways of horses with RAO in response to circulating catecholamines. SS-formoterol (10−8 to 10−5 M) facilitated ACh release in horses with RAO even in the absence of atropine. Addition of atropine did not cause significantly more augmentation of ACh release over the effect of SS-formoterol alone. The magnitude of augmentation in horses with RAO in the absence of atropine was similar to that in control horses in the presence of atropine. The latter observations could be explained by neuronal muscarinic-autoreceptor dysfunction in equine RAO.
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Takahashi, T., D. May, and C. Owyang. "Cholinergic dependence of gallbladder response to cholecystokinin in the guinea pig in vivo." American Journal of Physiology-Gastrointestinal and Liver Physiology 261, no. 4 (October 1, 1991): G565—G569. http://dx.doi.org/10.1152/ajpgi.1991.261.4.g565.
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The physiological mechanism responsible for cholecystokinin (CCK)-induced gallbladder (GB) contraction is unclear. We investigated the relative roles of direct muscle stimulation and neural activation at physiological and supraphysiological levels of CCK-octapeptide (CCK-8) using an in vivo guinea pig model. GB pressure was measured by a pressure transducer inserted into the GB lumen. Infusion of CCK-8 (2.5-40 ng.kg-1.min-1) increased GB pressure in a dose-dependent fashion. Pretreatment with atropine or hexamethonium antagonized GB responses to low doses of CCK-8 (2.5-5 ng.kg-1.min-1) but had no effect on doses greater than 10 ng.kg-1.min-1. Bilateral truncal vagotomy also significantly reduced GB responses to low doses of CCK-8 (2.5-5 ng.kg-1.min-1) but did not affect responses to high doses (10-40 ng.kg-1.min-1). Atropine or hexamethonium had no further inhibitory effects on guinea pigs that had undergone truncal vagotomy. Fasted guinea pigs that were fed ad libitum produced a postprandial peak plasma CCK level of 7.8 +/- 1.8 pM. This level was most closely approximated by infusion of 5 ng.kg-1.min-1 of CCK-8 (8.4 +/- 2.6 pM). CCK-8 infusion at greater than or equal to 10 ng.kg-1.min-1 gave supraphysiological plasma CCK levels. These observations indicate that CCK stimulated GB contraction via both a neural and a direct smooth muscle effect. Doses of CCK-8 that produce physiological plasma CCK levels act via stimulation of presynaptic cholinergic neurons in a vagally mediated pathway, whereas doses of CCK-8 that produce supraphysiological CCK levels act directly on GB smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)
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Davison, J. S., and A. Najafi-Farashah. "The distension stimulus to gastric acid secretion in the isolated mouse stomach." Canadian Journal of Physiology and Pharmacology 63, no. 12 (December 1, 1985): 1533–36. http://dx.doi.org/10.1139/y85-252.
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Distension of the isolated mouse stomach stimulated gastric acid secretion. Atropine, cimetidine, or proglumide antagonized the actions of cholinomimetics, histamine, and gastrin, respectively. However, these antagonists and the nerve blocking agent, tetrodotoxin, were without effect on basal secretion or distension-stimulated secretion. It is concluded that in the isolated mouse stomach neither basal secretion nor secretion evoked by distension involve the release of any of the established "physiological" secretagogues or the activation of intramural nerves.
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Fry, Jeffrey R., and Steven A. Burr. "A double-blind atropine trial for active learning of autonomic function." Advances in Physiology Education 35, no. 4 (December 2011): 438–44. http://dx.doi.org/10.1152/advan.00075.2011.
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Here, we describe a human physiology laboratory class measuring changes in autonomic function over time in response to atropine. Students use themselves as subjects, generating ownership and self-interest in the learning as well as directly experiencing the active link between physiology and pharmacology in people. The class is designed to concomitantly convey the importance of bias in experimentation by adopting a double-blind placebo-controlled approach. We have used this class effectively in various forms with ∼600 students receiving atropine over the last 16 yr. This class has received favorable feedback from staff and students of medicine, pharmacy, and neuroscience, and we recommend it for such undergraduates. The learning objectives that students are expected to achieve are to be able to 1) know the ethical, safety, and hygiene requirements for using human volunteers as subjects; 2) implement and explain a double-blind placebo-controlled trial; 3) design, agree, and execute a protocol for making (and accurately recording) precise reproducible measurements of pulse rate, pupil diameter, and salivary flow; 4) evaluate the importance of predose periods and measurement consistency to detect effects (including any reversibility) after an intervention; 5) experience direct cause-and-effect relationships integrating physiology with pharmacology in people; 6) calculate appropriate summary statistics to describe the data and determine the data's statistical significance; 7) recognize normal variability both within and between subjects in baseline physiological parameters and also recognize normal variability in response to pharmacological treatment; 8) infer the distribution and role of muscarinic receptors in the autonomic nervous system with respect to the heart, eye, and mouth; 9) identify and explain the clinical significance of differences in effect due to the route and formulation of atropine; 10) produce and deliver a concise oral presentation of experimental findings; and 11) produce a written report in the form of a short scientific research article. The results of a typical study are presented, which demonstrate that the administration of atropine by a subcutaneous injection elicited a significant increase in pulse rate and pupil diameter and a significant decrease in salivary flow, whereas administration of atropine in an oral liquid elicited significant effects on pulse rate and salivary flow, and an oral solid format elicited a significant alteration in salivary flow alone. More detailed analysis of the salivary flow data demonstrated clear differences between the routes of administration and formulation in the onset and magnitude of action of atropine.
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Ivanoff, A. Y., and P. A. Smith. "On the role of muscarinic and peptidergic receptors in ganglionic transmission in bullfrogs in vivo." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 5 (May 1, 1997): R1501—R1514. http://dx.doi.org/10.1152/ajpregu.1997.272.5.r1501.
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Synaptic activity of individual B and C cells in the paravertebral sympathetic ganglia of urethan-anesthetized bullfrogs was monitored with intracellular electrodes. Postganglionic activity from the B and C fiber populations was monitored with suction electrodes. Intravenous infusion of muscarine (0.1 ml of 8 microM) excited individual B cells and increased the amplitude and rate of spontaneous, postganglionic B fiber population discharges. Muscarine also increased the number of action potentials (APs) within each burst of synaptic activity in individual C cells. Because atropine (0.1 ml of 0.1 microM) had little or no effect on postganglionic population B or C fiber activity, the muscarinic slow inhibitory postsynaptic potentials and slow excitatory postsynaptic potentials (EPSPs) are unlikely to be involved in the transmission, modulation, or integration of postganglionic outflow in vivo. Atropine did, however, decrease the number of APs per burst in individual C cells, an effect that could be explained if excitatory presynaptic muscarinic receptors exist on C fiber terminals. Stimulation of preganglionic C fibers at "physiological" frequencies evoked a lasting afterdischarge in postganglionic B fibers that was blocked by a combination of atropine and [D-pyro-Glu1,D-Phe2,D-Trp3,6]-luteinizing hormone-releasing hormone (LHRH). Release of LHRH from C fiber terminals and activation of the peptidergic, late-slow EPSP mechanism in B cells may therefore play a role in ganglionic transmission in vivo.
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van Duijvenboden, Stefan, Ben Hanson, Nick Child, Michele Orini, Christopher A. Rinaldi, Jaswinder S. Gill, and Peter Taggart. "Effect of autonomic blocking agents on the respiratory-related oscillations of ventricular action potential duration in humans." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 12 (December 15, 2015): H2108—H2117. http://dx.doi.org/10.1152/ajpheart.00560.2015.
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Ventricular action potential duration (APD) is an important component of many physiological functions including arrhythmogenesis. APD oscillations have recently been reported in humans at the respiratory frequency. This study investigates the contribution of the autonomic nervous system to these oscillations. In 10 patients undergoing treatment for supraventricular arrhythmias, activation recovery intervals (ARI; a conventional surrogate for APD) were measured from multiple left and right ventricular (RV) endocardial sites, together with femoral artery pressure. Respiration was voluntarily regulated and heart rate clamped by RV pacing. Sympathetic and parasympathetic blockade was achieved using intravenous metoprolol and atropine, respectively. Metroprolol reduced the rate of pressure development (maximal change in pressure over time): 1,271 (± 646) vs. 930 (± 433) mmHg/s; P < 0.01. Systolic blood pressure (SBP) showed a trend to decrease after metoprolol, 133 (± 21) vs. 128 (± 25) mmHg; P = 0.06, and atropine infusion, 122 (± 26) mmHg; P < 0.05. ARI and SBP exhibited significant cyclical variations ( P < 0.05) with respiration in all subjects with peak-to-peak amplitudes ranging between 0.7 and 17.0 mmHg and 1 and 16 ms, respectively. Infusion of metoprolol reduced the mean peak-to-peak amplitude [ARI, 6.2 (± 1.4) vs. 4.4 (± 1.0) ms, P = 0.008; SBP, 8.4 (± 1.6) vs. 6.2 (± 2.0) mmHg, P = 0.002]. The addition of atropine had no significant effect. ARI, SBP, and respiration showed significant coupling ( P < 0.05) at the breathing frequency in all subjects. Directed coherence from respiration to ARI was high and reduced after metoprolol infusion [0.70 (± 0.17) vs. 0.50 (± 0.23); P < 0.05]. These results suggest a role of respiration in modulating the electrophysiology of ventricular myocardium in humans, which is partly, but not totally, mediated by β-adrenergic mechanisms.
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Latour, Martin G., and W. Wayne Lautt. "Insulin sensitivity regulated by feeding in the conscious unrestrained rat." Canadian Journal of Physiology and Pharmacology 80, no. 1 (January 1, 2002): 8–12. http://dx.doi.org/10.1139/y01-094.
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Hepatic insulin sensitizing substance (HISS), a putative hormone released from the liver in response to insulin in fed animals, accounts for 5060% of insulin action. HISS release is regulated by permissive control of the hepatic parasympathetic nerves. The objectives were to develop the rapid insulin sensitivity test (RIST) in conscious rats, and to assess the effects of anesthesia, atropine, feeding, and fasting on insulin action. The RIST index, expressed as milligrams glucose per kilogram body weight required to maintain euglycemia after a 50 mU/kg bolus of insulin, was similar in conscious and anesthetized rats (238.6 ± 42.5 vs. 225.3 ± 30.4 mg/kg). Atropine produced a 56% inhibition of insulin action in fed rats. After a 24 h fast, full HISS-dependent insulin resistance had developed as shown by a low RIST index that was not reduced further by atropine. Fasting caused a 10.5% decrease in insulin action per hour over six hours. HISS-dependent insulin resistance in 24-h fasted rats was reversed 4 h after re-feeding (90.9 ± 12.3 vs. 204.5 ± 30.5 mg/kg). We conclude that HISS-dependent and HISS-independent insulin action, as assessed by the RIST, is similar in conscious and pentobarbital-anesthetized rats. Pharmacological blockade of HISS-dependent insulin action and physiological regulation of HISS action by feedingfasting is confirmed. Re-feeding fasted rats reversed HISS-dependent insulin resistance. Merits of use of the RIST in conscious versus anesthetized rats are discussed.Key words: insulin action, insulin resistance, anesthetic effect, glucose, fasting, HISS.
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Barreto, Savio G., Colin J. Carati, Ann C. Schloithe, James Toouli, and Gino T. P. Saccone. "Galanin potentiates supramaximal caerulein-stimulated pancreatic amylase secretion via its action on somatostatin secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 6 (December 2009): G1268—G1273. http://dx.doi.org/10.1152/ajpgi.00342.2009.
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Galanin inhibits pancreatic amylase secretion from mouse lobules induced by physiological concentrations of caerulein via an insulin-dependent mechanism. We aimed to determine the effect and elucidate the mechanism of action of exogenous galanin on pancreatic amylase secretion induced by supramaximal concentrations of caerulein. Amylase secretion from isolated murine pancreatic lobules was measured. Lobules were coincubated with galanin (10−12–10−7 M) and caerulein (10−7 M). Lobules were preincubated with atropine (10−5 M), tetrodotoxin (10−5 M), diazoxide (10−7 M), or the galanin antagonist galantide (10−12–10−7 M) for 30 min followed by incubation with caerulein alone, or combined with galanin (10−12 M). Lobules were also coincubated with combinations of galanin (10−12 M), caerulein, octreotide (10−12–10−7 M) or cyclo-(7-aminoheptanoyl-Phe-D-Trp-Lys-Thr[BZL]), a somatostatin receptor antagonist (10−9 M). Amylase secretion was expressed as percent of total lobular amylase. Caerulein stimulated amylase secretion to 124% of control. Diazoxide pretreatment abolished the caerulein-stimulated amylase secretion, whereas atropine or tetrodotoxin caused a partial inhibition. Galanin (10−12–10−7 M) potentiated caerulein-stimulated amylase secretion to 160% of control. Preincubation with a combination of atropine and diazoxide abolished the potentiating effect of galanin, indicating muscarinic receptor and insulin mediation. Preincubation with galantide abolished the galanin effect, implying galanin receptor involvement. Coincubation with caerulein, galanin, and octreotide significantly reduced the potentiating effect galanin. However, coincubation with the somatostatin receptor antagonist, alone or in combination with galanin, significantly increased caerulein-stimulated amylase secretion to a level comparable to the galanin potentiation. Taken together, these data suggest that, at supramaximal caerulein concentrations, galanin acts via its receptors to further increase caerulein-stimulated amylase secretion by inhibiting the caerulein-induced release of somatostatin.
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Hicks, J. M., and A. P. Farrell. "The cardiovascular responses of the red-eared slider (Trachemys scripta) acclimated to either 22 or 5 degrees C. II. Effects of anoxia on adrenergic and cholinergic control." Journal of Experimental Biology 203, no. 24 (December 15, 2000): 3775–84. http://dx.doi.org/10.1242/jeb.203.24.3775.
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Cardiovascular control in cold-acclimated freshwater turtles during chronic anoxic exposure is not well understood. We tested the hypothesis that the observed bradycardia in Trachemys scripta results from increased cholinergic inhibitory tone and reduced sympathetic activity. Cardiovascular status was measured in vivo in turtles acclimated to either 22 degrees C or 5 degrees C and either acutely exposed (6 h) to anoxia at 22 degrees C or chronically exposed (22 days) to anoxia at 5 degrees C. In 22 degrees C-acclimated turtles, injection of the cholinergic antagonist atropine induced a significant tachycardia under both normoxic and anoxic conditions. However, in 5 degrees C-acclimated turtles, atropine injection had little effect on heart rate. Therefore, cholinergic control of heart rate was suppressed during cold acclimation; instead, temperature effects are more important in bringing about bradycardia, while the intrinsic effects of anoxia and acidosis are probably important during chronic anoxia. Injection of adrenaline caused a pressor response through increased systemic resistance at both acclimation temperatures. This response was blunted by acute and chronic anoxic exposure, suggesting that systemic vasomotor control was altered independently of acclimation temperature. This anoxic blunting may be related in part to the anoxia-induced increase in systemic resistance. Injection of nadolol after atropine decreased systemic cardiac output. The tonic beta-adrenergic cardiac stimulation was attenuated by acute and chronic anoxic exposure. Some of this attenuation of beta-adrenergic control could be attributed to the 39–40 % reduction in cell surface beta-adrenoreceptor density in the ventricles of these turtles that accompanied acute and chronic anoxic exposure. In conclusion and contrary to our original hypothesis, cholinergic and adrenergic control of the cardiovascular system in turtles was attenuated under cold anoxic conditions, perhaps assisting in the depressed physiological state of these animals.
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Ao, Yan, Vay Liang W. Go, Natalie Toy, Tei Li, Yu Wang, Moon K. Song, Joseph R. Reeve, Yanyun Liu, and Hong Yang. "Brainstem Thyrotropin-Releasing Hormone Regulates Food Intake through Vagal-Dependent Cholinergic Stimulation of Ghrelin Secretion." Endocrinology 147, no. 12 (December 1, 2006): 6004–10. http://dx.doi.org/10.1210/en.2006-0820.
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The brainstem is essential for mediating energetic response to starvation. Brain stem TRH is synthesized in caudal raphe nuclei innervating brainstem and spinal vagal and sympathetic motor neurons. Intracisternal injection (ic) of a stable TRH analog RX77368 (7.5–25 ng) dose-dependently stimulated solid food intake by 2.4- to 3-fold in freely fed rats, an effect that lasted for 3 h. By contrast, RX77368 at 25 ng injected into the lateral ventricle induced a delayed and insignificant orexigenic effect only in the first hour. In pentobarbital-anesthetized rats, RX77368 (50 ng) ic induced a significant bipeak increase in serum total ghrelin levels from the basal of 8.7 ± 1.7 ng/ml to 13.4 ± 2.4 ng/ml at 30 min and 14.5 ± 2.0 ng/ml at 90 min, which was prevented by either bilateral vagotomy (−60 min) or atropine pretreatment (2 mg/kg, −30 min) but magnified by bilateral adrenalectomy (−60 min). TRH analog ic-induced food intake in freely fed rats was abolished by either peripheral atropine or ghrelin receptor antagonist (d-Lys-3)-GHRP-6 (10 μmol/kg) or ic Y1 receptor antagonist 122PU91 (10 nmol/5 μl). Brain stem TRH mRNA and TRH receptor 1 mRNA increased by 57–58 and 33–35% in 24- and 48-h fasted rats and returned to the fed levels after a 3-h refeeding. Natural food intake in overnight fasted rats was significantly reduced by ic TRH antibody, ic Y1 antagonist, and peripheral atropine. These data establish a physiological role of brainstem TRH in vagal-ghrelin-mediated stimulation of food intake, which involves interaction with brainstem Y1 receptors.
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Montgomery, Laura E. A., Etain A. Tansey, Chris D. Johnson, Sean M. Roe, and Joe G. Quinn. "Autonomic modification of intestinal smooth muscle contractility." Advances in Physiology Education 40, no. 1 (March 2016): 104–9. http://dx.doi.org/10.1152/advan.00038.2015.
Full textAbstract:
Intestinal smooth muscle contracts rhythmically in the absence of nerve and hormonal stimulation because of the activity of pacemaker cells between and within the muscle layers. This means that the autonomic nervous system modifies rather than initiates intestinal contractions. The practical described here gives students an opportunity to observe this spontaneous activity and its modification by agents associated with parasympathetic and sympathetic nerve activity. A section of the rabbit small intestine is suspended in an organ bath, and the use of a pressure transducer and data-acquisition software allows the measurement of tension generated by the smooth muscle of intestinal walls. The application of the parasympathetic neurotransmitter ACh at varying concentrations allows students to observe an increase in intestinal smooth muscle tone with increasing concentrations of this muscarinic receptor agonist. Construction of a concentration-effect curve allows students to calculate an EC50 value for ACh and consider some basic concepts surrounding receptor occupancy and activation. Application of the hormone epinephrine to the precontracted intestine allows students to observe the inhibitory effects associated with sympathetic nerve activation. Introduction of the drug atropine to the preparation before a maximal concentration of ACh is applied allows students to observe the inhibitory effect of a competitive antagonist on the physiological response to a receptor agonist. The final experiment involves the observation of the depolarizing effect of K+ on smooth muscle. Students are also invited to consider why the drugs atropine, codeine, loperamide, and botulinum toxin have medicinal uses in the management of gastrointestinal problems.
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Hamambulu, Pharaoh, Fastone Mathew-Goma, Newton Simfukwe, Lukubi Lwiindi, and Kwangu Chitembusha-Mwenya. "Effects of Steganotaenia Araliacae Root Extract on Contractile Function of Isolated Rat Ileum." Journal of Preventive and Rehabilitative Medicine 3, no. 2 (June 1, 2021): 32–41. http://dx.doi.org/10.21617/jprm2021.328issn.
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Background: Various parts of a small tree, Steganotaenia araliacaeare used as medicine in local traditional settings in Zambia to initiate and augment parturition although very little is documented about its physiological and pharmacological effects. Steganotaenia araliacaecold extract has been observed to cause contractions of uterus in rats but its effect on non-uterine muscle is unclear. The aim of this study was to establish the contractile effect of Steganotaenia araliacaecold extract on isolated rat ileum smooth muscle.Method: Animals were sacrificed by cervical dislocation. Abdominal incisions were made to expose and dissect three ileum segments from each rat. The ileum segments were immediately transferred and mounted in the organ bath containing Tyrode solution. The contractile effects of acetylcholine (a reference agonist) and Steganotaenia araliacaecold extract on ileum segments were investigated starting with the least effective doses, thereafter doubling the doses until maximal tissue response was observed. Antagonists that include atropine, indomethacin, mepyramine, ondansetron and nifedipine in the presence and absence of Steganotaenia araliacaecold extract were also investigated to establish the mechanism of actionResults: Steganotaenia araliacaecold extract increased the contractile force of isolated rat ileum in a dose-response manner but had no significant effects on the frequency of the spontaneous contractions. Pre-treating the tissue with atropine, indomethacin, mepyramine or ondansetron did not inhibit the contractile force of Steganotaenia araliacaecold extract, while pre-treating the tissue with nifedipine inhibited its contractile force by 100% (p<0.05)Conclusion: The cold root extract of Steganotaenia araliacae induced contractions on isolated rat ileum smooth muscle in a dose response manner by probable activation of calcium channels. It is possible that SAEᶜif used in high doses may cause severe abdominal cramps an effect that needs to be noted as it is being used in parturition.
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Dacey, R. G., and J. E. Bassett. "Cholinergic vasodilation of intracerebral arterioles in rats." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 5 (November 1, 1987): H1253—H1260. http://dx.doi.org/10.1152/ajpheart.1987.253.5.h1253.
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Much morphological and physiological evidence indicates that cholinergic mechanisms play a significant role in the control of cerebral blood flow. Despite in situ data suggesting that an intrinsic cholinergic mechanism produces vasodilation in the intracerebral microcirculation, there is no direct information on the effect of acetylcholine (ACh) on intracerebral arterioles. We investigated cholinergic mechanisms in isolated perfused intracerebral arterioles from pentobarbital sodium-anesthetized Sprague-Dawley rats. In arterioles with resting diameters of 46.8 +/- 6.6 microns (mean +/- SE) ACh produced no significant dilation at pH 7.30. At pH 7.60, however, a significant dose-dependent dilation to a maximum of 119.0 +/- 1.0% of control diameter was observed. Carbachol, a long-acting cholinergic agonist, similarly failed to dilate vessels at pH 7.30 but significantly dilated vessels at pH 7.60. Prostaglandin F2 alpha produced a maximum contraction to 68.3 +/- 2.7% of control diameter (n = 8). ACh at concentrations of 10(-4) and 2 X 10(-4) M induced a significant dilation of this prostaglandin-induced contraction. In vessels similarly preconstricted with serotonin, 10(-4) M ACh produced significant dilation. Atropine, having no effect on vessel diameter when administered alone, blocked cholinergic vasodilation of intracerebral arterioles at pH 7.60. Attempts at endothelial removal, although successful in eliminating endothelial cells from the preparation, significantly impaired smooth muscle contractility. ACh has no significant effect on the spontaneous cerebrovascular tone in this preparation, but in vessels preconstricted by a variety of means it produced vasodilation mediated by atropine sensitive receptors.
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Storr, M., E. Gaffal, D. Saur, V. Schusdziarra, and H. D. Allescher. "Effect of cannabinoids on neural transmission in rat gastric fundus." Canadian Journal of Physiology and Pharmacology 80, no. 1 (January 1, 2002): 67–76. http://dx.doi.org/10.1139/y02-005.
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The purpose of this study was to examine the possible role of cannabinoids on the neuromuscular function of rat gastric fundus. In addition to possible direct effects on smooth muscle, the influence of cannabinoids on contractile (cholinergic) and relaxant (non-adrenergic, non-cholinergic (NANC)) neural innervation of the rat gastric fundus was investigated in vitro. Neither anandamide (an endogenous cannabinoid receptor agonist) nor Win 55,212-2 and methanandamide (synthetic cannabinoid receptor agonists) nor AM 630 (a cannabinoid receptor antagonist) showed any effect on smooth muscle activity at baseline or after precontraction with 5-hydroxytryptamine (5-HT; 107 M). Electrical field stimulation (EFS) of the smooth muscle preparation (40 V; 5 Hz) caused cholinergically mediated twitch contractions that were abolished by atropine (106 M) or tetrodotoxin (TTX; 106 M). Anandamide and Win 55,212-2 reduced these twitch contractions in a concentration-dependent manner, an effect that could be reversed by the cannabinoid receptor antagonist AM 630 for anandamide, but not for Win 55,212-2. When NANC relaxant neural responses (presence of atropine (106 M) and guanethidine (106 M)) were induced by EFS, the cannabinoid receptor agonists anandamide and Win 55,212-2 reduced the relaxant response, an effect that could be reversed by the cannabinoid receptor antagonist AM 630 for anandamide, but not for Win 55,212-2. When given alone AM 630 caused an increase in the EFS-induced relaxant response. The presence of CB1 and CB2 cannabinoid receptor mRNA within the rat stomach was demonstrated by reverse transcription polymerase chain reaction (RT-PCR). The results of this study indicate that cannabinoids modulate excitatory cholinergic and inhibitory NANC neurotransmission in the rat gastric fundus. Endogenous cannabinoids may play a physiological role only in NANC inhibitory transmission, as AM 630 did not modify the electrically induced cholinergic contraction. The involved cannabinoid receptors are most likely located on neuronal structures. The present study also provides evidence that more than one receptor type is involved.Key words: cannabinoid, anandamide, rat gastric fundus relaxation, NANC, AM 630.
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BISHT, DEVENDER SINGH, NARENDRA SINGH JADON, DEEPTI BODH, and MANJUL KANDPAL. "Clinicophysiological and haematobiochemical effects of dexmedetomidinepropofol-sevoflurane anaesthesia in dogs." Indian Journal of Animal Sciences 88, no. 8 (September 6, 2018): 887–91. http://dx.doi.org/10.56093/ijans.v88i8.82910.
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The present study was conducted to evaluate the clinicophysiological and haematobiochemical effects of dexmedetomidine in dogs undergoing propofol-sevoflurane anaesthesia. Twelve apparently healthy adult dogs were divided into two groups having 6 animals each. Animals of group I received atropine sulphate @ 0.04 mg/kg s.c. + dexmedetomidine @ 10 μg/kg i.v. while animals of group II were administered atropine sulphate @ 0.04 mg/ kg s.c. + dexmedetomidine @ 15 μg/kg i.v. Anaesthesia was induced with propofol (as i.v. bolus till effect) and maintained with sevoflurane. Clinicophysiological and haematobiochemical parameters were recorded at different intervals. Quicker attenuation of clinical reflexes was observed in both groups. Induction time was significantly lower while duration of anaesthesia, recovery time, standing time, complete recovery time and percent reduction in MAC of sevoflurane was significantly higher in group II. Non-significant differences in induction dose of propofol, physiological and haematobiochemical parameters were observed in both groups. Significant decrease in heart rate, respiration rate, rectal temperature, haemoglobin oxygen saturation and significant increase in mean arterial pressure was recorded in both the groups. Transient significant decrease in haemoglobin, total leukocyte count, total erythrocyte count and transient significant increase in glucose, urea nitrogen, creatinine, alanine aminotransferase, aspartate aminotransferase and cortisol was recorded in both the groups. Erythrocyte sedimentation rate increased significantly while insulin level decreased significantly in both groups. Both anaesthetic combinations used in the present study produced satisfactory anaesthesia and muscle relaxation, therefore can be suggested for clinical use in canine patients undergoing propofol-sevoflurane anaesthesia.
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Jones, C. J., C. L. Bell, and P. M. Quinton. "Different physiological signatures of sweat gland secretory and duct cells in culture." American Journal of Physiology-Cell Physiology 255, no. 1 (July 1, 1988): C102—C111. http://dx.doi.org/10.1152/ajpcell.1988.255.1.c102.
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Human eccrine sweat gland cells grown in culture were found to lose their characteristic shape, becoming flattened and organized into multilayers. The resting membrane potentials of the cultured secretory cells (-35 +/- 2 mV, n = 36) were significantly higher than those measured for cultured duct cells (-22 +/- 1 mV, n = 58, P less than or equal to 0.01). When the cholinergic agonist methacholine (10(-5) or 10(-6) M) was administered, the cultured secretory cells could be distinguished unequivocally by their atropine-sensitive hyperpolarizing response (-20 +/- 2 mV, n = 43), whereas no cultured duct cells responded. When the sodium conductance antagonist amiloride (10(-5) or 10(-6) M) was administered, 44% of cultured secretory cells responded by hyperpolarization (-8 +/- 1 mV, n = 8), whereas 87% of cultured duct cells hyperpolarized (-15 +/- 1 mV, n = 46) and by a significantly greater margin (P less than or equal to 0.01). Substitution of chloride with gluconate in the bathing medium caused membrane potential depolarization in both cultured secretory and duct cell populations, which is consistent with the presence of a chloride conductance in the plasma membrane. The beta-adrenoceptor agonist isoproterenol induced a transient hyperpolarization of 5-10 mV in three out of six cultured secretory cells tested but had no effect on cultured duct cells.
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Yaksh, Tony L., Jia-Yi Wang, V. L. W. Go, and Gail J. Harty. "Cortical Vasodilatation Produced by Vasoactive Intestinal Polypeptide (VIP) and by Physiological Stimuli in the Cat." Journal of Cerebral Blood Flow & Metabolism 7, no. 3 (June 1987): 315–26. http://dx.doi.org/10.1038/jcbfm.1987.69.
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In chloralose-urethanized cats, vasoactive intestinal peptide (VIP), applied by superfusion in steady-state concentration (10−10–10−6 M) onto cortical vessels in situ resulted in a rapid concentration-dependent vasodilatation in vessels that were mildly constricted by prostaglandin F2α (PGF2α) (5 × 10−5 M) or hypocarbia (PaCO2 = 26). The maximum dilatation produced by VIP (10−6 M) was about 60% over baseline in pial arteries and 40% in pial veins. Blockade of local neuronal activity with tetrodotoxin (TTX) (10−5 M) had no effect on the VIP-evoked dilation of pial vessels. Activation of the cortex by either direct electrical stimulation or indirectly by stimulation of the mesencephalic reticular formation (MRF) resulted in a rapid dilatation of pial arterioles and venules. The vasodilatory effects of VIP and of cortical activation via direct cortical stimulation were not blocked by phentolamine (10−4 M), propranolol (10−4 M), atropine (10−4 M), or naloxone (10−4 M), indicating that the stimulated vasodilatation was not mediated by adrenergic, cholinergic, or opiate receptors. The dilatory effects of MRF, but not direct cortical stimulation, were not blocked by TTX. VIP antiserum (1:25) preincubated in cortical cups had no effect on resting vessel diameter, but resulted in a significant, though subtotal, reduction in the vasodilatation elicited by direct cortical and MRF stimulation. Normal rabbit sera or VIP antiserum preincubated with saturating amounts of VIP were ineffective. In similar experiments, pial arteriolar and venular dilation evoked by hypercarbia was not attenuated by cortically applied VIP antisera. These observations suggest that pial dilation evoked by local increases in neuronal activity may be mediated in part by the local release of VIP from intrinsic neurons. Such a substrate would define a close obligatory coupling between local neuronal activation and local perfusion, such that nutritive flow could be enhanced prior to the onset of any metabolic deficit.
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Just, Armin, Jörg Faulhaber, and Heimo Ehmke. "Autonomic cardiovascular control in conscious mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2214—R2221. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2214.
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Autonomic cardiovascular control was characterized in conscious, chronically catheterized mice by spectral analysis of arterial pressure (AP) and heart rate (HR) during autonomic blockade or baroreflex modulation of autonomic tone. Both spectra were similar to those obtained in humans, but at ∼10× higher frequencies. The 1/ f relation of the AP spectrum changed to a more shallow slope below 0.1–0.2 Hz. Coherence between AP and HR reached 0.5 or higher below 0.3–0.4 Hz and also above 2.5 Hz. Muscarinic blockade (atropine) or β-adrenergic blockade (atenolol) did not significantly affect the AP spectrum. Atropine reduced HR variability at all frequencies, but this effect waned above 1 Hz. β-Adrenergic blockade (atenolol) slightly enhanced the HR variability only above 1 Hz. α-Adrenergic blockade (prazosin) reduced AP variability between 0.05 and 3 Hz, most prominently at 0.15–0.7 Hz. A shift of the autonomic nervous tone by a hypertensive stimulus (phenylephrine) enhanced, whereas a hypotensive stimulus (nitroprusside) depressed AP variability at 1–3 Hz; other frequency ranges of the AP spectrum were not affected except for a reduction below 0.4 Hz after nitroprusside. Variability of HR was enhanced after phenylephrine at all frequencies and reduced after nitroprusside. As with atropine, the reduction with nitroprusside waned above 1 Hz. In conclusion, in mice HR variability is dominated by parasympathetic tone at all frequencies, during both blockade and physiological modulation of autonomic tone. There is a limitation for further reduction but not for augmentation of HR variability from the resting state above 1 Hz. The impact of HR on AP variability in mice is confined to frequencies higher than 1 Hz. Limits between frequency ranges are proposed as 0.15 Hz between VLF (very low frequency range) and LF (low frequency range) and 1.5 Hz between LF and HF (high frequency range).
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Nelson, D. K., B. Glasbrenner, G. Dahmen, R. L. Riepl, P. Malfertheiner, and G. Adler. "M1 muscarinic mechanisms regulate intestinal-phase gallbladder physiology in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 5 (November 1, 1996): G824—G830. http://dx.doi.org/10.1152/ajpgi.1996.271.5.g824.
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The contribution of muscarinic receptor subtypes to biliary control mechanisms is unclear. We investigated stimulated gallbladder function and release of associated hormones during M1-receptor blockade. Following a double-blind, randomized, crossover protocol, healthy volunteers each received placebo and telenzepine, a selective M1-receptor antagonist, as 2-h background infusion. Gallbladder contraction (by ultrasonography), bilirubin output, and release of cholecystokinin (CCK) and pancreatic polypeptide (PP) were assessed during increasing doses of endogenous (intraduodenal nutrient) and exogenous (hormonal) stimulation. All parameters were stimulated in a dose-dependent manner on placebo days. Contractile and secretory responses to low-dose caerulein (CCK analogue) were inhibited by 60–80% under telezepine, whereas high-dose (supraphysiological) stimulation overrode this effect. Similar inhibition was achieved during nutrient stimulation. CCK plasma levels rose during endogenous and exogenous stimulation but were unaffected by M1 blockade, whereas stimulated PP release was completely inhibited (< 100% decrease), reflecting suppressed vagal tone. Selective M1-receptor blockade inhibits the physiological response of the gallbladder in humans; this effect cannot be attributed to suppressed CCK release. Our findings support the hypothesis that CCK acts at the gallbladder via cholinergic nerves under physiological conditions. Viewed with our previous observations, nonselective antagonism of biliary function by atropine is primarily mediated through M1 muscarinic pathways.
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Hernandez, I., and J. Chacin. "Mechanism of cholinergic stimulation of glucose oxidation in isolated gastric glands." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 2 (August 1, 1994): G227—G234. http://dx.doi.org/10.1152/ajpgi.1994.267.2.g227.
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The mechanisms of cholinergic activation of carbohydrate metabolism were investigated in isolated rabbit gastric glands. Carbachol stimulated the rate of glucose oxidation in a dose-dependent fashion with a half-maximal effect occurring at approximately 9 microM. Atropine and omeprazole, but not cimetidine, completely blocked the stimulation induced by carbachol. Direct activation of the H(+)-K(+)-adenosinetriphosphatase by NH+4 caused a significant stimulation of glucose oxidation that was totally abolished by oligomycin and by the mitochondrial uncouplers dinitrophenol and carbonyl cyanide p-trifluoromethoxyphenylhydrazone. These latter agents did not abolish the stimulating effect of carbachol on glucose oxidation. Ionomycin increased the rate of glucose oxidation in a dose-dependent manner, and this effect was not blocked by oligomycin. The metabolic effect of ionomycin was reduced but not abolished by omeprazole. 1,2-Bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester eliminated the carbachol-induced stimulation of glucose oxidation and partially inhibited the effect of NH+4. The mitochondrial enzymes pyruvate dehydrogenase and oxoglutarate dehydrogenase were activated by physiological concentrations of calcium in the isolated mitochondria. This effect was blocked by incubation with ruthenium red.(ABSTRACT TRUNCATED AT 250 WORDS)
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Tenore, Gian, Ester Pagano, Stefania Lama, Daniela Vanacore, Salvatore Di Maro, Maria Maisto, Raffaele Capasso, et al. "Intestinal Anti-Inflammatory Effect of a Peptide Derived from Gastrointestinal Digestion of Buffalo (Bubalus bubalis) Mozzarella Cheese." Nutrients 11, no. 3 (March 13, 2019): 610. http://dx.doi.org/10.3390/nu11030610.
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Under physiological conditions, the small intestine represents a barrier against harmful antigens and pathogens. Maintaining of the intestinal barrier depends largely on cell–cell interactions (adherent-junctions) and cell–matrix interactions (tight-junctions). Inflammatory bowel disease is characterized by chronic inflammation, which induces a destructuring of the architecture junctional epithelial proteins with consequent rupture of the intestinal barrier. Recently, a peptide identified by Bubalus bubalis milk-derived products (MBCP) has been able to reduce oxidative stress in intestinal epithelial cells and erythrocytes. Our aim was to evaluate the therapeutic potential of MBCP in inflammatory bowel disease (IBD). We studied the effect of MBCP on (i) inflamed human intestinal Caco2 cells and (ii) dinitrobenzene sulfonic acid (DNBS) mice model of colitis. We have shown that MBCP, at non-cytotoxic concentrations, both in vitro and in vivo induced the adherent epithelial junctions organization, modulated the nuclear factor (NF)-κB pathway and reduced the intestinal permeability. Furthermore, the MBCP reverted the atropine and tubocurarine injury effects on adherent-junctions. The data obtained showed that MBCP possesses anti-inflammatory effects both in vitro and in vivo. These results could have an important impact on the therapeutic potential of MBCP in helping to restore the intestinal epithelium integrity damaged by inflammation.
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Baroody, F. M., M. Wagenmann, and R. M. Naclerio. "Comparison of the secretory response of the nasal mucosa to methacholine and histamine." Journal of Applied Physiology 74, no. 6 (June 1, 1993): 2661–71. http://dx.doi.org/10.1152/jappl.1993.74.6.2661.
Full textAbstract:
To better understand the secretory response of the nasal mucosa, we must be able to accurately measure its physiological response. To this end, we developed a localized challenge technique using paper disks to stimulate the mucosa on one side and measure secretions from both sides to study both direct and reflex responses. Both methacholine and histamine induced a dose-dependent increase in secretion weights on the challenge side, whereas only histamine induced a contralateral reflex. Repeated stimulation with histamine, but not methacholine, resulted in tachyphylaxis. Pretreatment with atropine resulted in inhibition of the contralateral secretory response to histamine and the ipsilateral response to methacholine with only partial inhibition of the ipsilateral histamine response. Terfenadine pretreatment resulted in the complete inhibition of both the ipsilateral and contralateral responses to histamine with no effect on methacholine anduced secretions. Ipsilaterally applied lidocaine had no effect on the histamine response but, when applied contralaterally, partially inhibited that response. Topical diphenhydramine applied ipsilaterally led to significant inhibition of the ipsilateral and contralateral secretory responses to histamine but had no effect when applied contralaterally. We conclude that methacholine and histamine have different effects on the nasal mucosa. We speculate that methacholine stimulates glands directly, whereas histamine includes both direct and neurogenic stimulation.
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Von Scheidt, W., M. Bohm, A. Stablein, G. Autenrieth, and E. Erdmann. "Antiadrenergic effect of M-cholinoceptor stimulation on human ventricular contractility in vivo." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 6 (December 1, 1992): H1927—H1931. http://dx.doi.org/10.1152/ajpheart.1992.263.6.h1927.
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The relevance of an indirect negative inotropic effect of pharmacological or vagally mediated M-cholinoceptor stimulation in the human ventricle in vivo is unknown. The inotropic response induced by isoproterenol (isoprenaline, 20 ng.kg-1 x min-1), measured by m-mode echocardiography as the increase of fractional shortening in seven healthy subjects, was reduced from 17.1 +/- 4.3 to 9.1 +/- 3.9% (P < 0.01) by M-cholinoceptor stimulation using intravenous injection of 3.6 micrograms/kg carbachol. However, the inotropic response of increasing doses of isoprenaline (5-20 ng.kg-1 x min-1) did not differ in 13 healthy subjects without and after M-cholinoceptor blockade (atropine, 0.015 mg/kg i.v.); the increase of fractional shortening amounted to 17.4 +/- 4.0 vs. 19.5 +/- 4.8% (NS) in response to 20 ng.kg-1 x min-1 isoprenaline. It is concluded that pharmacological M-cholinoceptor stimulation of the human ventricle significantly reduces the inotropic response of beta-adrenoceptor stimulation. This may offer a new therapeutic approach to attenuate an increased cardiac sympathetic tone. However, M-cholinoceptor blockade, i.e., interruption of parasympathetic influences, does not augment the inotropic response to beta-adrenoceptor stimulation. Therefore, in healthy resting humans a physiological role of the parasympathetic nervous system in mediating an indirect negative inotropic effect on ventricular contractility seems to be absent.
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Kwon, Hyeok Y., Ta-Min Chang, Kae Y. Lee, and William Y. Chey. "Vagus nerve modulates secretin binding sites in the rat forestomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 4 (April 1, 1999): G1052—G1058. http://dx.doi.org/10.1152/ajpgi.1999.276.4.g1052.
Full textAbstract:
Secretin is well known for its inhibitory action on gastric motility. It has been reported that secretin in a physiological dose inhibits gastric motility through mediation by the vagal afferent pathway. Secretin also elicited relaxation of carbachol-stimulated rat forestomach muscle strips by binding to its receptors, suggesting a direct action on this peripheral tissue. We hypothesized that vagal input may affect the action of secretin by modulating the level of secretin receptor in the forestomach. Several treatments, including vagal ligation, vagotomy, perivagal application of capsaicin or colchicine, intravenous infusion of tetrodotoxin, and intraperitoneal injection of atropine, were performed to investigate their effects on secretin receptor binding to forestomach membranes. Specific binding of125I-labeled secretin to forestomach membranes was significantly decreased (45%) by vagal ligation, vagotomy (50%), or perivagal colchicine treatment (40%). On the contrary, specific binding of125I-secretin was not affected by perivagal capsaicin treatment, intravenous infusion of tetrodotoxin, or intraperitoneal injection of atropine. By Scatchard analysis of the binding data, the capacity of the high-affinity binding sites in forestomach membranes was found to decrease significantly after vagal ligation compared with membranes from the sham-operated group. However, the affinity at the high-affinity binding sites, the binding parameters of the low-affinity binding sites, and binding specificity were not changed. Vagal ligation but not perivagal capsaicin treatment reduced the inhibitory effect of secretin on bethanechol-stimulated contraction of isolated forestomach muscle strips, causing a right shift in the dose-response curve. These results suggest that vagal input through axonal transport plays a significant role on secretin action by modulating the capacity of secretin binding sites (but not affinity or specificity), at least in rat forestomach.
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Fukumoto, Satoshi, Makoto Tatewaki, Tadanori Yamada, Mineko Fujimiya, Chris Mantyh, Miranda Voss, Steve Eubanks, Mary Harris, Theodore N. Pappas, and Toku Takahashi. "Short-chain fatty acids stimulate colonic transit via intraluminal 5-HT release in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 5 (May 1, 2003): R1269—R1276. http://dx.doi.org/10.1152/ajpregu.00442.2002.
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We studied whether physiological concentration of short-chain fatty acids (SCFAs) affects colonic transit and colonic motility in conscious rats. Intraluminal administration of SCFAs (100–200 mM) into the proximal colon significantly accelerated colonic transit. The stimulatory effect of SCFAs on colonic transit was abolished by perivagal capsaicin treatment, atropine, hexamethonium, and vagotomy, but not by guanethidine. The stimulatory effect of SCFAs on colonic transit was also abolished by intraluminal pretreatment with lidocaine and a 5-hydroxytryptamine (HT)3 receptor antagonist. Intraluminal administration of SCFAs provoked contractions at the proximal colon, which migrated to the mid- and distal colon. SCFAs caused a significant increase in the luminal concentration of 5-HT of the vascularly isolated and luminally perfused rat colon ex vivo. It is suggested that the release of 5-HT from enterochromaffin cells in response to SCFAs stimulates 5-HT3 receptors located on the vagal sensory fibers. The sensory information is transferred to the vagal efferent and stimulates the release of acetylcholine from the colonic myenteric plexus, resulting in muscle contraction.
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Tamori, Keisuke, Masashi Yoneda, Kimihide Nakamura, and Isao Makino. "Effect of intracisternal thyrotropin-releasing hormone on hepatic blood flow in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 2 (February 1, 1998): G277—G282. http://dx.doi.org/10.1152/ajpgi.1998.274.2.g277.
Full textAbstract:
Central neuropeptides play a role in many physiological regulatory processes through the autonomic nervous system. Thyrotropin-releasing hormone (TRH) is distributed in the central nervous system and acts as a neurotransmitter to regulate gastric functions through vagal-muscarinic pathways. The central effect of the TRH analog on hepatic blood flow was investigated in urethan-anesthetized rats. Hepatic blood flow was determined by the hydrogen gas clearance technique. Intracisternal injection of the stable TRH analog RX-77368 (5–100 ng) dose dependently increased hepatic blood flow with peak response at 15 min after the peptide was administered (net change from basal for vehicle and 5, 10, 100, and 500 ng RX-77368 was 2.0 ± 0.2, 8.9 ± 0.8, 19.4 ± 2.6, 32.6 ± 3.3, and 28.5 ± 6.8 ml ⋅ min−1 ⋅ 100 g−1, respectively), and this stimulatory effect returned to baseline at 90 min. The stimulation of hepatic blood flow by the intracisternally administered TRH analog was abolished by atropine methyl nitrate (0.15 mg/kg ip), indomethacin (5 mg/kg ip), N G-nitro-l-arginine methyl ester (10 mg/kg iv), and hepatic branch vagotomy but not by cervical spinal cord transection (C6 level). Intravenous injection of RX-77368 did not have any effect on hepatic blood flow. These results indicate that TRH acts in the central nervous system to stimulate hepatic blood flow through vagal-muscarinic and indomethacin- and nitric oxide-dependent pathways.
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Wang, Norman C., Alexandru Chicos, Smriti Banthia, Daniel W. Bergner, Marc K. Lahiri, Jason Ng, Haris Subačius, Alan H. Kadish, and Jeffrey J. Goldberger. "Persistent sympathoexcitation long after submaximal exercise in subjects with and without coronary artery disease." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 3 (September 2011): H912—H920. http://dx.doi.org/10.1152/ajpheart.00148.2011.
Full textAbstract:
There is an increased risk of cardiac events after exercise, which may, in part, be mediated by the sympathoexcitation that accompanies exercise. The duration and extent of this sympathoexcitation following moderate exercise is unknown, particularly in those with coronary artery disease (CAD). Twenty control subjects (mean age, 51 years) and 89 subjects with CAD (mean age, 58 years) underwent two 16-min bicycle exercise sessions followed by 30–45 min of recovery. Session 1 was performed under physiological conditions to peak workloads of 50–100 W. In session 2, parasympathetic blockade with atropine (0.04 mg/kg) was achieved at end exercise at the same workload as session 1. RR interval was continually recorded, and plasma catecholamines were measured at rest and selected times during exercise and recovery. Parasympathetic effect, measured as the difference in RR interval with and without atropine, did not differ between controls and CAD subjects in recovery. At 30 and 45 min of recovery, RR intervals were 12% and 9%, respectively, shorter than at rest. At 30 and 45 min of recovery, plasma norepinephrine levels were 15% and 12%, respectively, higher than at rest. A brief period of moderate exercise is associated with a prolonged period of sympathoexcitation extending >45 min into recovery and is quantitatively similar among control subjects and subjects with CAD, with or without left ventricular dysfunction. Parasympathetic reactivation occurs early after exercise and is also surprisingly quantitatively similar in controls and subjects with CAD. The role of these autonomic changes in precipitating cardiac events requires further evaluation.
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Ming, Zhi, and W. Wayne Lautt. "HISS, not insulin, causes vasodilation in response to administered insulin." Journal of Applied Physiology 110, no. 1 (January 2011): 60–68. http://dx.doi.org/10.1152/japplphysiol.00714.2010.
Full textAbstract:
Meal-induced sensitization to the dynamic actions of insulin results from the peripheral actions of a hormone released by the liver (hepatic insulin sensitizing substance or HISS). Absence of meal-induced insulin sensitization results in the pathologies associated with cardiometabolic risk. Using three protocols that have previously demonstrated HISS metabolic action, we tested the hypothesis that HISS accounts for the vasodilation that has been associated with insulin. The dynamic metabolic actions of insulin and HISS were determined using a euglycemic clamp in response to a bolus of 100 mU/kg insulin in pentobarbital-anesthetized Sprague-Dawley rats. Hindlimb blood flow was measured with an ultrasound flow probe on the aorta above the bifurcation of the iliac arteries. Fed rats showed tightly coupled metabolic and vascular responses, which were completed by 35 min after insulin administration. Blocking HISS release, with the use of atropine or hepatic surgical denervation, eliminated the HISS-dependent metabolic and vascular responses to insulin administration. Physiological suppression of HISS release occurs with fasting. In 24-h fasted rats, HISS metabolic and vascular actions were absent, and atropine had no effect on either action. Fed rats with liver denervation did not release HISS, but intraportal venous infusion of acetylcholine, to mimic the permissive parasympathetic nerve signal, restored the ability of insulin to cause HISS release and restored both the metabolic and vascular actions. These studies report vascular actions of HISS for the first time and demonstrate that HISS, not insulin action, results in the peripheral vasodilation generally attributed to insulin.
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Nakade, Yukiomi, Rena Kitano, Taeko Yamauchi, Satoshi Kimoto, Kazumasa Sakamoto, Tadahisa Inoue, Yuji Kobayashi, et al. "Effect of Central Corticotropin-Releasing Factor on Hepatic Lipid Metabolism and Inflammation-Related Gene Expression in Rats." International Journal of Molecular Sciences 22, no. 8 (April 11, 2021): 3940. http://dx.doi.org/10.3390/ijms22083940.
Full textAbstract:
Corticotropin-releasing factor (CRF) in the brain acts on physiological and pathophysiological modulation of the hepatobiliary system. Central CRF administration aggravates experimental acute liver injury by decreasing hepatic blood flow. Conversely, minimal evidence is available regarding the effect of centrally acting CRF on hepatic lipid metabolism and inflammation. We examined whether central CRF affects hepatic lipid metabolism and inflammation-related gene expression in rats. Male Long Evans rats were intracisternally injected with CRF (10 μg) or saline. Rats were sacrificed 2 h, 6 h, and 24 h after the CRF injection, the liver was isolated, and mRNA was extracted. Next, hepatic lipid metabolism and inflammation-related gene expression were examined. Hepatic SREBF1 (sterol regulatory element-binding transcription factor 1) mRNA levels were significantly increased 6 h and 24 h after intracisternal CRF administration when compared with those in the control group. Hepatic TNFα and IL1β mRNA levels increased significantly 6 h after intracisternal CRF administration. Hepatic sympathectomy or guanethidine treatment, not hepatic branch vagotomy or atropine treatment, inhibited central CRF-induced increase in hepatic SREBF1, TNFα and IL1β mRNA levels. These results indicated that central CRF affects hepatic de novo lipogenesis and inflammation-related gene expression through the sympathetic-noradrenergic nervous system in rats.
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Wetzel, G. T., and J. H. Brown. "Presynaptic modulation of acetylcholine release from cardiac parasympathetic neurons." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 1 (January 1, 1985): H33—H39. http://dx.doi.org/10.1152/ajpheart.1985.248.1.h33.
Full textAbstract:
Acetylcholine can be released from parasympathetic nerve endings in rat atria by 57 mM K+ depolarization or by electrical field stimulation. We have studied the presynaptic modulation of [3H]acetylcholine release from superfused rat atria prelabeled with [3H]choline. Exogenous acetylcholine and the specific muscarinic agonist oxotremorine inhibit the stimulation-induced overflow of [3H]acetylcholine into the superfusion medium. The half-maximal inhibitory concentration (IC50) of oxotremorine is 0.3 microM. The cholinesterase inhibitor neostigmine also decreases K+-stimulated [3H]acetylcholine overflow, whereas the muscarinic antagonist atropine enhances the overflow of [3H]acetylcholine. These data suggest that acetylcholine release in atria is modulated through negative feedback by the endogenous transmitter. The sympathetic adrenergic neurotransmitter norepinephrine and the neurohormone epinephrine also inhibit the overflow of [3H]acetylcholine by approximately 60%. The IC50 values for the inhibitory effects of these catecholamines are 6.3 and 2.2 microM, respectively. The inhibitory effect of norepinephrine is blocked by the alpha-adrenergic receptor antagonist yohimbine but not by the beta-adrenergic receptor antagonist propranolol. We suggest that presynaptic muscarinic and alpha-adrenergic receptors participate in the physiological and pharmacological control of cardiac parasympathetic activity.
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Fox, J. E., and E. E. Daniel. "Substance P: a potent inhibitor of the canine small intestine in vivo." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 1 (January 1, 1986): G21—G27. http://dx.doi.org/10.1152/ajpgi.1986.250.1.g21.
Full textAbstract:
Intra-arterially administered substance P inhibited neurally activated contractions of the circular muscle of canine small intestine in vivo (lowest effective dose approximately 10(-13) mol). Excitation of intestine required higher (10(-10) mol) doses. The inhibitory effect required functioning nerves, since tetrodotoxin treatment eliminated it. However, inhibition of neurogenic contraction by substance P was unaffected by nicotinic or opiate receptor antagonists or by catecholamine depletion but was reduced by a selective substance P antagonist. Since the inhibition by substance P was also greatly reduced by treatment with atropine or pirenzepine and acetylcholine given intra-arterially produced a similar inhibitory response, stimulation of release of acetylcholine to inhibitory muscarinic receptors on nerves appeared to be the mechanism of this action. Direct smooth muscle effects were ruled out; substance P did not inhibit contractions to intra-arterial acetylcholine or those following tetrodotoxin. In vitro in ileal strips, no inhibition by substance P of any contractile response was found. We propose that the local release of substance P into the myenteric plexus produces inhibition and suggest that this constitutes a physiological function of the neuropeptide. This action may be absent in vitro.
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Arsene, Mea, Kouakou, Abo, Nguessa, Irie Bi, and Kahou Bi. "MYOSTIMULANT EFFECT OF LEAVES OF CASSIA OCCIDENTALIS (CAESALPINIACEAE) ON ISOLATED RABBIT DUODENUM." International Journal of Research -GRANTHAALAYAH 5, no. 4 (April 30, 2017): 301–10. http://dx.doi.org/10.29121/granthaalayah.v5.i4.2017.1824.
Full textAbstract:
The fresh leaves of Cassia occidentalis are used in the African pharmacopoeia to treat constipation and malaria. This practice is not recommended for pregnant women. In traditional medicine the fresh leaves used in enema would have abortive properties.
In this work, the aqueous extract of dry leaves of Cassia occidentalis (AECo) is added to the Mc Ewan type physiological solution containing the isolated intestine muscle which is suspended between two shaped stainless steel hooks.
Doses of AECo less than 10-2 mg / ml have no significant effect on duodenal contractions.
For doses between 10-1 mg / ml and 4 mg / ml, baseline amplitude and tone increased from 10.12 ± 4.02% (P <0.005) to 55.37 ± 3.23% (P <0.001).
Indeed, at doses of 1, 2 and 4 mg / ml, AECo leads to significant increases in the amplitude of the contractions which pass successively from 0.32 ± 0.09 mN, 0.41 ± 0.07 mN to 0.49 ± 0, 13 mN (P <0.001).
Let a variation in the amplitude of the rhythmic contractions of the duodenum of 30.82 ± 3.07%, 44.32 ± 2.47% and 55.37 ± 4.23%, respectively. An increase in the amplitude and tone of rhythmic contractions is in a dose-dependent manner.
The myostimulant effect is characterized by the increase of the rhythm and the amplitude of isolated intestine muscle.
The effect of AECo is partially suppressed by atropine. This suggests the presence of muscarinic cholinergic compounds in this aqueous extract.
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Yokohama, Shiro, Masashi Yoneda, Kimihide Nakamura, and Isao Makino. "Effect of central corticotropin-releasing factor on carbon tetrachloride-induced acute liver injury in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 3 (March 1, 1999): G622—G628. http://dx.doi.org/10.1152/ajpgi.1999.276.3.g622.
Full textAbstract:
Central neuropeptides play important roles in many instances of physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Stressors and sympathetic nerve activation are reported to exacerbate experimental liver injury. Some stressors are known to stimulate corticotropin-releasing factor (CRF) synthesis in the central nervous system and induce activation of sympathetic nerves in animal models. The effect of intracisternal CRF on carbon tetrachloride (CCl4)-induced acute liver injury was examined in rats. Intracisternal injection of CRF dose dependently enhanced elevation of the serum alanine aminotransferase (ALT) level induced by CCl4. Elevations of serum aspartate aminotransferase, alkaline phosphatase, and total bilirubin levels by CCl4were also enhanced by intracisternal CRF injection. Intracisternal injection of CRF also aggravated CCl4-induced hepatic histological changes. Intracisternal CRF injection alone did not modify the serum ALT level. Intravenous administration of CRF did not influence CCl4-induced acute liver injury. The aggravating effect of central CRF on CCl4-induced acute liver injury was abolished by denervation of hepatic plexus with phenol and by denervation of noradrenergic fibers with 6-hydroxydopamine treatment but not by hepatic branch vagotomy or atropine treatment. These results suggest that CRF acts in the brain to exacerbate acute liver injury through the sympathetic-noradrenergic pathways.
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LILIOM, Károly, Guoping SUN, Moritz BÜNEMANN, Tamás VIRÁG, Nóra NUSSER, Daniel L. BAKER, De-an WANG, et al. "Sphingosylphosphocholine is a naturally occurring lipid mediator in blood plasma: a possible role in regulating cardiac function via sphingolipid receptors." Biochemical Journal 355, no. 1 (February 26, 2001): 189–97. http://dx.doi.org/10.1042/bj3550189.
Full textAbstract:
Blood plasma and serum contain factors that activate inwardly rectifying GIRK1/GIRK4 K+ channels in atrial myocytes via one or more non-atropine-sensitive receptors coupled to pertussis-toxin-sensitive G-proteins. This channel is also the target of muscarinic M2 receptors activated by the physiological release of acetylcholine from parasympathetic nerve endings. By using a combination of HPLC and TLC techniques with matrix-assisted laser desorption ionization–time-of-flight MS, we purified and identified sphingosine 1-phosphate (SPP) and sphingosylphosphocholine (SPC) as the plasma and serum factors responsible for activating the inwardly rectifying K+ channel (IK). With the use of MS the concentration of SPC was estimated at 50nM in plasma and 130nM in serum; those concentrations exceeded the 1.5nM EC50 measured in guinea-pig atrial myocytes. With the use of reverse-transcriptase-mediated PCR and/or Western blot analysis, we detected Edg1, Edg3, Edg5 and Edg8 as well as OGR1 sphingolipid receptor transcripts and/or proteins. In perfused guinea-pig hearts, SPC exerted a negative chronotropic effect with a threshold concentration of 1µM. SPC was completely removed after perfusion through the coronary circulation at a concentration of 10µM. On the basis of their constitutive presence in plasma, the expression of specific receptors, and a mechanism of ligand inactivation, we propose that SPP and SPC might have a physiologically relevant role in the regulation of the heart.
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Schuessler, R. B., T. E. Canavan, J. P. Boineau, and J. L. Cox. "Baroreflex modulation of heart rate and initiation of atrial activation in dogs." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 3 (September 1, 1988): H503—H513. http://dx.doi.org/10.1152/ajpheart.1988.255.3.h503.
Full textAbstract:
In open-chest dogs, blood pressure was regulated by titrating doses of phenylephrine and nitroprusside to determine its effect on heart rate and pacemaker location. Changes in blood pressure correlated with changes in heart rate (r = 0.86). Activation time mapping demonstrated multicentric atrial activation, with a site of origin-rate relationship. The fastest pacemakers were located in the most cranial regions and slowest in the most caudal areas. In this chloralose-morphine anesthetized model, autonomic blockade with atropine and propranolol suggests that acute baroreflex-induced changes in heart rate were mediated exclusively by either increased sympathetic or parasympathetic tone and were not associated with inhibition of the opposite system. Division of right and left thoracic cardiac nerves indicated the left sympathetics participated in the baroreflex in 50% of the animals and the left parasympathetics in 90% of the animals. Both the right sympathetics and parasympathetics were active in the baroreflex in all animals. The data demonstrate that physiological heart rate response is regulated through an extensive system of right atrial pacemakers modulated by both left and right efferent cardiac nerves.
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Feldman, M. "Gastric H+ and HCO3- secretion in response to sham feeding in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 248, no. 2 (February 1, 1985): G188—G191. http://dx.doi.org/10.1152/ajpgi.1985.248.2.g188.
Full textAbstract:
Sham feeding (SF) was used to evaluate the effect of physiological vagal stimulation on gastric acid (H+) and bicarbonate (HCO3-) secretion in humans, as well as on parietal and nonparietal volume secretion. A recently validated method, derived from a two-component model of gastric secretion, was employed. SF increased both H+ secretion from parietal cells (P less than 0.001) and HCO3- secretion from nonparietal cells (P less than 0.01), although the H+ response was greater and more prolonged. Atropine significantly inhibited not only H+ secretion but also HCO3- and nonparietal volume secretion. Peak H+ secretion during SF averaged approximately 27 mmol/h, whereas peak HCO3- secretion averaged approximately 6 mmol/h. When H+ secretion was already maximally stimulated by an intravenous pentagastrin infusion, SF actually reduced gastric juice acidity and osmolality due to neutralization of H+ by HCO3- and to dilution of H+ by nonparietal secretions. These studies therefore indicate that vagal stimulation induced by SF increases both H+ and HCO3- secretion in humans and that this process is cholinergically dependent.
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Schulze-Delrieu, K., and S. S. Shirazi. "Pressure and length adaptations in isolated cat stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 252, no. 1 (January 1, 1987): G92—G99. http://dx.doi.org/10.1152/ajpgi.1987.252.1.g92.
Full textAbstract:
Correlations were made between the adaptation of gastric pressure and longitudinal muscle tension. Isolated cat stomachs were filled with physiological solution and longitudinal strips marked in five segments over the lesser and the greater curvature (LC and GC). Strip length changed the most in the proximal segments of GC. Volume changes led to triphasic changes in gastric pressure. On filling, there was a pressure peak and pressure accommodation to a new base-line pressure. On emptying there was an initial pressure nadir that was followed by a pressure recovery. When isolated longitudinal strips were stretched and released to their lengths at specific gastric volumes, they generated triphasic tension adaption and recovery. Strips from the proximal greater curvature generated the highest base-line tension, highest peak tension, and largest amplitude of tension adaptations. Addition of KCl, carbachol, or physostigmine increased base-line tension and tension adaptations in parallel, whereas atropine reduced them. Tetrodotoxin had no effect. The base-line tension of the isolated cat stomach is maintained by a tonic cholinergic neurosecretion but its tension adaptations do not require neural control.
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Miao, L., Z. Qiu, and J. P. Morgan. "Cholinergic stimulation modulates negative inotropic effect of cocaine on ferret ventricular myocardium." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 2 (February 1, 1996): H678—H684. http://dx.doi.org/10.1152/ajpheart.1996.270.2.h678.
Full textAbstract:
We tested the hypothesis that the negative inotropic effect (NIE) of cocaine is mediated, at least in part, by cholinergic stimulation and can be correlated with the degree of adenosine 3',5'-cyclic monophosphate (cAMP) dependency of the inotropic state. Cardiac myocytes were isolated from left ventricles of ferrets and loaded with the fluorescent Ca2+ indicator indo 1. Cells were placed in physiological solution containing 2.0 mM Ca2+ and stimulated at 0.5 Hz and 30 degrees C. Cocaine decreased peak cell shortening and peak intracellular Ca2+ in a concentration-dependent manner (10(-8)-10(-4) M). The concentration-response curve of cocaine was shifted significantly downward compared with those of lidocaine and procaine in the same range of concentrations. Atropine (10(-6) M) shifted the concentration-response curve of cocaine, but not those of lidocaine and procaine, rightward, with a pA2 value (7.66) similar to that obtained with carbachol (7.99). With prior addition of isoproterenol (ISO, 10(-8) M) or increased Ca2+ (4.0 mM) to increase cell shortening to the same degree (approximately 60%), cocaine and carbachol decreased contractility to a significantly greater extent in ISO-stimulated myocytes. To clarify whether these treatments changed responsiveness of the contractile elements to Ca2+, the effect of 2,3-butanedione monoxime, an agent that interferes with the interaction of myosin and actin, was tested with previous addition of ISO or increased Ca2+, and no differential effect occurred. Therefore, we postulate that 1) the NIE of cocaine on myocytes is caused by decreased Ca2+ availability; 2) this effect is due to specific stimulation of cholinergic receptors in addition to other direct myocardial (probably local anesthetic) effects; and 3) the NIE correlates with the level of cAMP dependence of the inotropic state.
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Maunder, E. M. W., A. V. Pillay, and A. D. Care. "Endocrine control of plasma concentrations of calcium-binding protein in the pig." Journal of Endocrinology 115, no. 1 (October 1987): 121–28. http://dx.doi.org/10.1677/joe.0.1150121.
Full textAbstract:
ABSTRACT The aetiology of the rise in plasma calbindin-D9k (vitamin D-induced calcium-binding protein; CaBP), following insulin-induced hypoglycaemia, was studied in the pig. ACTH led to a rise in plasma concentrations of both CaBP and cortisol. Metyrapone, which blocks cortisol synthesis, abolished the increases in plasma concentrations of CaBP and cortisol normally observed in response to insulin-induced hypoglycaemia. However, there was no significant rise in plasma concentrations of CaBP in response to pharmacological or physiological doses of cortisol. Injection of clonidine, an α2-adrenergic agonist, led to a rise in plasma concentrations of CaBP, whereas phenylephrine, an α1-adrenergic agonist, tended to exert an inhibitory effect. Also, administration of phentolamine (an α-adrenergic blocker) before injection of insulin abolished the usual increase in plasma concentrations of CaBP, whereas propranolol (a β-adrenergic blocker) enhanced the normal increase in plasma concentrations of CaBP in response to insulin-induced hypoglycaemia. Isoproterenol, a β-adrenergic agonist, was without effect on plasma CaBP. Neither GH nor glucagon appear to be involved in the rise in plasma CaBP following insulin-induced hypoglycaemia. Although atropine abolished the effect of acute hypoglycaemia on plasma CaBP, carbamylcholine was without effect on plasma CaBP concentration. It is concluded that the increases in plasma CaBP induced by either ACTH or α2-adrenergic stimulation may be interrelated since the administration of ACTH can lead to raised plasma concentrations of catecholamines. J. Endocr. (1987) 115, 121–128
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HARDIE, ROGER C. "Effects of Antagonists on Putative Histamine Receptors in the First Visual Neuropile of the Housefly (Musca Domestica)." Journal of Experimental Biology 138, no. 1 (September 1, 1988): 221–41. http://dx.doi.org/10.1242/jeb.138.1.221.
Full textAbstract:
Intracellular recordings were made from the large monopolar cells (LMCs), which are the cells postsynaptic to photoreceptors, in the housefly Musca domestica. A multi-barrelled ionophoretic pipette glued to the recording electrode was used to apply a variety of cholinergic and histaminergic antagonists onto the recorded neurones. All substances which blocked the physiological response to light also antagonized the response to ionophoretically applied histamine, supporting the hypothesis that histamine is the neurotransmitter released by insect photoreceptors. In order of potency, the following drugs were found to block or reduce the LMCs responses to light: benzoquinonium ≥ gallamine > ranitidine ≥ atropine ≊ cimetidine > metiamide≊SK&F93479 ≥ mepyramine. Mecamylamine, scopolamine, dexetimide, nicotine, mequitazine, chlorpheniramine and clemastine were ineffective. Two other cholinergic ligands, hexamethonium and decamethonium, were much more potent than even benzoquinonium, but had the effect of facilitating and greatly slowing down the responses to light. Responses evoked by acetylcholine showed a different pharmacology, being blocked by mecamylamine but unaffected by hexamethonium. Despite testing a number of known cholinergic and histaminergic agents, no effective agonist for histamine was found. The results indicate the existence of a novel class of histamine-sensitive receptor with nicotinic features. In addition the unusual effects of a traditional HI agonist, 2-thiazolylethylamine, suggested the presence of a second, distinct class of histamine receptor.
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Thiruchelvam, N., C. Wu, A. David, A. S. Woolf, P. M. Cuckow, and C. H. Fry. "Neurotransmission and viscoelasticity in the ovine fetal bladder after in utero bladder outflow obstruction." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 5 (May 1, 2003): R1296—R1305. http://dx.doi.org/10.1152/ajpregu.00688.2002.
Full textAbstract:
Fetal bladder outflow obstruction, predominantly caused by posterior urethral valves, results in significant urinary tract pathology; these lesions are the commonest cause of end-stage renal failure in children, and up to 50% continue to suffer from persistent postnatal bladder dysfunction. To investigate the physiological development of the fetal bladder and the response to urinary flow impairment, we performed partial urethral obstruction and complete urachal ligation in the midgestation fetal sheep for 30 days. By electrical and pharmacological stimulation of bladder strips, we found that muscarinic, purinergic, and nitrergic mechanisms exist in the developing fetal bladder at this gestation. After bladder outflow obstruction, the fetal bladder became hypocontractile, producing less force after nerve-mediated and muscarinic stimulation with suggested denervation, and also exhibited greater atropine resistance. Furthermore, fetal bladder urothelium exerted a negative inotropic effect, partly nitric oxide mediated, that was not present after obstruction. Increased compliance, reduced elasticity, and viscoelasticity were observed in the obstructed fetal bladder, but the proportion of work performed by the elastic component (a physical parameter of extracellular matrix) remained the same. In addition to denervation, hypocontractility may result from a reduction in the elastic modulus that may prevent any extramuscular components from sustaining force produced by detrusor smooth muscle.
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Boutsiouki, Paraskevi, and Geraldine F. Clough. "Modulation of microvascular function following low-dose exposure to the organophosphorous compound malathion in human skin in vivo." Journal of Applied Physiology 97, no. 3 (September 2004): 1091–97. http://dx.doi.org/10.1152/japplphysiol.00123.2004.
Full textAbstract:
This study investigates whether malathion, a widely used organophosphate insecticide, has its effects on cutaneous vasculature in healthy human volunteers through its anticholinergic activity or through the modulation of other, noncholinergic pathways. Acute, low-dose exposure to malathion (10 mg/ml for 5 h under occlusive dressing) caused a significant increase in cutaneous blood flux, monitored by using laser-Doppler flowmetry and imaging. It had little effect on tissue levels of ACh, nitric oxide, and histamine assayed in dermal dialysate collected from malathion-exposed and control-treated skin. The duration of the cutaneous vascular response to exogenous ACh (2%) delivered by iontophoresis was significantly enhanced by preexposure to malathion, both <1 h after its removal and 24 h later ( P < 0.001). At <1 h, the time to 50% decay of the response was 24 ± 4 and 50 ± 8 min in control and malathion-treated skin, respectively. Malathion also enhanced the size and duration of the axon reflex-mediated vasoresponse to ACh. The increase in blood flux to malathion and the endothelium-mediated response to exogenous ACh, both in the presence and absence of malathion, were attenuated by pretreatment of the skin with atropine and local anesthesia ( P < 0.01). We conclude that short-term exposure to a single low dose of malathion causes prolonged modulation of the physiological function of the cutaneous vasculature and that this is, in part, through its action on acetylcholinesterase at both neuronal and nonneuronal sites.
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Donald, J. A., J. E. O'Shea, and H. B. Lillywhite. "Somatostatin and innervation of the heart of the snake Elaphe obsoleta." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 4 (April 1, 1990): R1001—R1007. http://dx.doi.org/10.1152/ajpregu.1990.258.4.r1001.
Full textAbstract:
The innervation of the heart of the snake Elaphe obsoleta was examined with peptide immunohistochemistry, glyoxylic acid-induced catecholamine fluorescence, and in vitro physiological preparations. Snakes were anesthetized with Nembutal. Many somatostatin (SOM)-like immunoreactive (LI) axons were observed in the sinus venosus, atria, and ventricle. Cell bodies with SOM-LI were found in the intracardiac nerve trunks of the sinus venosus, the interatrial septum, and the atrioventricular region. The SOM-LI axons and cell bodies were not affected by 6-hydroxy-dopamine and capsaicin. They are probably intrinsic parasympathetic neurons. Adrenergic, neuropeptide Y-LI, substance P-LI, and calcitonin gene-related peptide-LI axons were found in the sinus venosus, atria, and ventricle. In spontaneously beating sinoatrial or electrically driven atrial preparations, applied SOM (6 x 10(-9) M and 6 x 10(-8) M) decreased the force of atrial contraction and/or the rate of beating. The effects of SOM were tachyphylactic. SOM had no effect on the force of contraction of the driven ventricle. Stimulation of the left and right vagus nerves elicited negative chronotropic and inotropic responses followed by poststimulus positive inotropic and chronotropic responses. Atropine abolished the inhibition, and bretylium abolished the excitation. After cholinergic and adrenergic blockade, high-frequency vagal nerve stimulation had no effect on heart rate and the force of contraction. Thus, although there is an extensive distribution of intrinsic SOM-LI neurons in the heart and although applied SOM is a potent inhibitor of rate and force, SOM in the vagal neurons does not appear to act as a direct inhibitory transmitter to the cardiac muscle or pacemaker cells.
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Ruzicka, Bianca B., and Khem Jhamandas. "Depression of potassium-evoked striatal acetylcholine release by δ-receptor activation: inhibition by cholinoactive agents." Canadian Journal of Physiology and Pharmacology 66, no. 12 (December 1, 1988): 1487–92. http://dx.doi.org/10.1139/y88-243.
Full textAbstract:
To examine the role of δ-opioid receptors in the modulation of striatal acetylcholine (ACh) release, the action of D-Pen2,L-Pen5-enkephalin, a selective δ-opioid receptor agonist, was tested on [3H]ACh release from slices of the rat caudate–putamen. Slices, incubated with [3H]choline, were superfused with a physiological buffer and stimulated twice by exposure to a high potassium (K+) concentration. In the absence of a cholinesterase inhibitor, 1 μM D-Pen2,L-Pen5-enkephalin produced a 46 and 35% decrease in the release of [3H]ACh evoked by 15 and 25 mM K+, respectively. The depressant action of the enkephalin analogue was concentration dependent, with a maximal effect on K+-evoked [3H]ACh release occurring at 1.0 μM, and was completely blocked in the presence of the δ-opioid receptor selective antagonist, ICI 174864 (1 μM). In the presence of the cholinesterase inhibitors physostigmine (10 μM) and neostigmine (10 μM), or the muscarinic receptor agonist oxotremorine (10 μM), D-Pen2,L-Pen5-enkephalin did not depress the K+-evoked release of [3H]ACh. Atropine (1 μM) blocked the inhibitory effect of physostigmine on the depressant action of D-Pen2,L-Pen5-enkephalin. The results of this study indicate that δ-opioid receptor activation is associated with an inhibition of striatal ACh release, but this opioid–cholinergic interaction is not apparent under conditions of presynaptic muscarinic receptor activation.