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1
Barnea, Eytan R., Rina Perlman, Hassan Fakih, Tova Bick, Shahar Kol, and Zeev Hochberg. "The role of catecholamines in estradiol and progesterone secretion by cultured explants and cells of human term placentae." Acta Endocrinologica 121, no. 6 (December 1989): 767–72. http://dx.doi.org/10.1530/acta.0.1210767.
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Abstract. The effects of physiological concentrations of the native catecholamines norepinephrine and epinephrine upon term placental hormonal function were examined by measuring estradiol and progesterone secretion by organ and cell culture systems. Results show that, in explants, both catecholamines caused a significant increase in the secretion of both sex steroids, p < 0.05. Estradiol secretion was blocked by the alpha and beta adrenergic receptors antagonists, phenoxybenzamine and propranolol, respectively, p < 0.05. Norepinephrine but not epinephrine dependent progesterone secretion was blocked by propranolol. In cells, epinephrine stimulated cyclic AMP generation and caused a 30% increase in estradiol secretion, p < 0.05. Both were abrogated by propranolol. Norepinephrine increased secretion by 25%, p < 0.05. This was inhibited by yohimbin and prazosin, alpha-1 and -2 receptors antagonists, respectively. In conclusion, the placenta in vitro is a target organ for catecholamines. The marked response of the explant system as compared with the marginal response of the cell culture system indicates that cell to cell contact/communication is required for full expression of catecholamine effect.
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Haas, M., and T. J. McManus. "Effect of norepinephrine on swelling-induced potassium transport in duck red cells. Evidence against a volume-regulatory decrease under physiological conditions." Journal of General Physiology 85, no. 5 (May 1, 1985): 649–67. http://dx.doi.org/10.1085/jgp.85.5.649.
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Duck red cells exhibit specific volume-sensitive ion transport processes that are inhibited by furosemide, but not by ouabain. Swelling cells in a hypotonic synthetic medium activates a chloride-dependent, but sodium-independent, potassium transport. Shrinking cells in a hypertonic synthetic medium stimulates an electrically neutral co-transport of [Na + K + 2 Cl] with an associated 1:1 K/K (or K/Rb) exchange. These shrinkage-induced modes can also be activated in both hypo- and hypertonic solutions by beta-adrenergic catecholamines (e.g., norepinephrine). Freshly drawn cells spontaneously shrink approximately 4-5% when removed from the influence of endogenous plasma catecholamines, either by incubation in a catecholamine-free, plasma-like synthetic medium, or in plasma to which a beta-receptor blocking dose of propranolol has been added. This spontaneous shrinkage resembles the response of hypotonically swollen cells in that it is due to a net loss of KCl with no change in cell sodium. Norepinephrine abolishes the net potassium transport seen in both fresh and hypotonically swollen cells. Moreover, cells swollen in diluted plasma, at physiological pH and extracellular potassium, show no net loss of KCl and water ("volume-regulatory decrease") unless propranolol is added. Examination of the individual cation fluxes in the presence of catecholamines demonstrates that activation of [Na + K + 2Cl] co-transport with its associated K/Rb exchange prevents, or overrides, swelling-induced [K + Cl] co-transport. These results, therefore, cast doubt on whether the swelling-induced [K + Cl] system can serve a volume-regulatory function under in vivo conditions.
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Keating, Damien J., and Chen Chen. "Activin A stimulates catecholamine secretion from rat adrenal chromaffin cells: a new physiological mechanism." Journal of Endocrinology 186, no. 2 (August 2005): R1—R5. http://dx.doi.org/10.1677/joe.1.06301.
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Activin A is a member of the transforming growth factor-β family and has known roles in the adrenal cortex, from which activin A is secreted. We aimed to find whether activin A induces secretion of catecholamines from chromaffin cells of the adrenal medulla, which neighbours the adrenal cortex in vivo. Using carbon fibre amperometry, we were able to measure catecholamine secretion in real-time from single chromaffin cells dissociated from the rat adrenal medulla. Activin A stimulated catecholamine secretion in a rapid and dose-dependent manner from chromaffin cells. This effect was fully reversible upon washout of activin A. The minimum dose at which activin A had a maximal effect was 2 nM, with an EC50 of 1.1 nM. The degree of secretion induced by activin A (2 nM) was smaller than that due to membrane depolarization caused by an increase in the external K+ concentration from 5 to 70 mM. No response to activin A was seen when Ca2+ channels were blocked by Cd2+ (200 μM). We conclude from these findings that activin A is capable of stimulating a robust level of catecholamine secretion from adrenal chromaffin cells in a concentration-dependent manner. This occurs via the opening of voltage-gated Ca2+ channels, causing Ca2+ entry, thereby triggering exocytosis. These findings illustrate a new physiological role of activin A and a new mechanism in the control of catecholamine secretion from the adrenal medulla.
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Mayerhofer, A., RW Steger, G. Gow, and A. Bartke. "Catecholamines stimulate testicular testosterone release of the immature golden hamster via interaction with alpha- and beta-adrenergic receptors." Acta Endocrinologica 127, no. 6 (December 1992): 526–30. http://dx.doi.org/10.1530/acta.0.1270526.
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Several lines of evidence suggest that catecholamines are involved in the regulation of the development of the testis. We have therefore investigated the ability of testicular parenchyma (decapsulated pieces of testes) from 18 to 20-day-old golden hamsters to respond to catecholaminergic stimuli in vitro. Norepinephrine and epinephrine, as well as the beta-receptor agonist isoproterenol and the alpha-adrenoreceptor agonist phenylephrine were able to significantly stimulate testicular testosterone production. Dopamine and serotonin were not effective. The stimulatory action of norepinephrine on testosterone production was dependent on the concentration. In incubations of testes with human chorionic gonadotropin (hCG) and norepinephrine, no synergistic effects on testosterone release were observed. The stimulatory effect of norepinephrine could be partially blocked by incubation with beta-receptor antagonist propranolol, or with alpha-receptor antagonist prazosin, while a combination of propranolol and prazosin completely inhibited the norepinephrine-induced testosterone production. Moreover, isoproterenol and phenylephrine in combination stimulated testosterone more than either drug did alone. Measurements of concentrations of norepinephrine and epinephrine in testicular homogenates revealed higher values for these catecholamines than in the plasma, implying that catecholamine levels in the interstitial spaces of the testis might be in the range of concentrations effectively stimulating testosterone production in vitro. This suggests that in the immature testis of the golden hamster, catecholamines acting through both alpha- and beta-adrenergic receptors may be potent physiological stimulators of testosterone production.
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Fulop, Tiberiu, and Corey Smith. "Physiological stimulation regulates the exocytic mode through calcium activation of protein kinase C in mouse chromaffin cells." Biochemical Journal 399, no. 1 (September 13, 2006): 111–19. http://dx.doi.org/10.1042/bj20060654.
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Adrenal medullary chromaffin cells release catecholamines and neuropeptides in an activity-dependent manner controlled by the sympathetic nervous system. Under basal sympathetic tone, catecholamines are preferentially secreted. During acute stress, increased sympathetic firing evokes release of both catecholamines as well as neuropeptides. Both signalling molecules are co-packaged in the same large dense core granules, thus release of neuropeptide transmitters must be regulated after granule fusion with the cell surface. Previous work has indicated this may be achieved through a size-exclusion mechanism whereby, under basal sympathetic firing, the catecholamines are selectively released through a restricted fusion pore, while less-soluble neuropeptides are left behind in the dense core. Only under the elevated firing experienced during the sympathetic stress response do the granules fully collapse to expel catecholamines and neuropeptides. However, mechanistic description and physiological regulation of this process remain to be determined. We employ electrochemical amperometry, fluid-phase dye uptake and electrophysiological capacitance noise analysis to probe the fusion intermediate in mouse chromaffin cells under physiological electrical stimulation. We show that basal firing rates result in the selective release of catecholamines through an Ω-form ‘kiss and run’ fusion event characterized by a narrow fusion pore. Increased firing raises calcium levels and activates protein kinase C, which then promotes fusion pore dilation until full granule collapse occurs. Our results demonstrate that the transition between ‘kiss and run’ and ‘full collapse’ exocytosis serves a vital physiological regulation in neuroendocrine chromaffin cells and help effect a proper acute stress response.
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Perry, S. F., R. Fritsche, and S. Thomas. "STORAGE AND RELEASE OF CATECHOLAMINES FROM THE CHROMAFFIN TISSUE OF THE ATLANTIC HAGFISH MYXINE GLUTINOSA." Journal of Experimental Biology 183, no. 1 (October 1, 1993): 165–84. http://dx.doi.org/10.1242/jeb.183.1.165.
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A variety of in vivo and in situ experiments were performed on the Atlantic hagfish (Myxine glutinosa) (i) to characterize the levels of circulating catecholamines during acute stresses, including hypoxia, anoxia or physical disturbance (air-exposure), and (ii) to evaluate the potential mechanisms of catecholamine release from the major sites of storage, the systemic heart and posterior cardinal vein (PCV). Adrenaline and noradrenaline were stored at roughly equivalent concentrations (approximately 20 microgram g-1) in cardiac tissue, whereas noradrenaline was the predominant catecholamine stored in the PCV (approximately 50 microgram g-1). The heart stored larger quantities of total catecholamines than did the PCV (approximately three times greater) owing to its larger mass and higher concentration of adrenaline. Exposure of chronically cannulated hagfish to acute hypoxia [mean water PO2 (PwO2)=1.4 kPa; 10.5 mmHg) for 30 min caused a significant decrease in arterial PO2 (from 11.5+/−1.3 kPa to 1.2+/−0.3 kPa) and arterial O2 content (from 3.9+/−0.3 ml 100 ml-1 to 0.9+/−0.2 ml 100 ml-1). The hypoxaemia was associated with a significant increase in plasma noradrenaline levels, whereas plasma adrenaline levels were unaffected. Exposure of uncannulated fish to anoxia (PwO2 approximately 0 kPa) or physical disturbance (15 min of air-exposure) also elicited pronounced increases in plasma noradrenaline levels (6–10 times) and, to a lesser extent, adrenaline levels (2–3 times). An in situ saline-perfused heart preparation was utilized in an attempt to elucidate the mechanism(s) underlying the stress-induced release of catecholamines from the chromaffin tissue of the heart and PCV. Non-specific cell membrane depolarization using 40 or 60 mmol l-1 K+ in the saline elicited a marked release of catecholamines, confirming the suitability of the preparation to assess specific physiological mechanisms of catecholamine release. Lower concentrations of K+ (15–20 mmol l-1) did not evoke catecholamine release, indicating that relatively minor elevation in plasma [K+], as might occur during hypoxia, is not a contributing factor. The cholinergic receptor agonist carbachol (10–5-10-4 mol kg-1) caused a significant release of catecholamines, yet the likelihood of a similar mechanism operating in vivo is doubtful because the hagfish heart is not thought to be innervated. Simulation of (i) internal hypoxaemia by perfusing with anoxic saline or (ii) physical disturbance by perfusing with relatively acidic saline (pH approximately 7.0) failed to elicit catecholamine release. Further, the elevation of perfusion (input) pressure to simulate a rise in venous blood pressure, as might occur during hypoxia or physical disturbance, was also without effect on release. The addition of pituitary extract (from Atlantic cod, Gadus morhua) to the inflowing saline caused a marked release of catecholamines from the chromaffin tissue.
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Fritsche, R., S. G. Reid, S. Thomas, and S. F. Perry. "SEROTONIN-MEDIATED RELEASE OF CATECHOLAMINES IN THE RAINBOW TROUT ONCORHYNCHUS MYKISS." Journal of Experimental Biology 178, no. 1 (May 1, 1993): 191–204. http://dx.doi.org/10.1242/jeb.178.1.191.
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The effects of serotonin (5-hydroxytryptamine; 5-HT) on catecholamine release from chromaffin tissue were investigated in the rainbow trout (Oncorhynchus mykiss) in vivo and in situ. Intra-arterial injections of serotonin in vivo caused dose-dependent (50–250 nmol kg-1) increases in both plasma noradrenaline and adrenaline levels. Pre-treatment of fish with the serotonergic receptor antagonist methysergide did not abolish these increases. An in situ saline-perfused head kidney preparation was developed and validated to study the potential direct effect of serotonin on catecholamine release. The chromaffin cells in the preparation showed a dose-dependent release of catecholamines in response to bolus injections of the cholinergic receptor agonist carbachol (10–7-10-4 mol kg-1). The carbachol-induced release of noradrenaline, but not of adrenaline, was reduced significantly when the nicotinic receptor antagonist hexamethonium (10–4 mol l-1) was present in the perfusion fluid. The removal of calcium from the perfusion fluid prevented the usual release of catecholamines evoked by carbachol. Bolus injections of serotonin (250 nmol kg-1) into the inflowing perfusion fluid resulted in significantly increased levels of adrenaline and noradrenaline in the outflowing perfusate. Addition of hexamethonium to the perfusion fluid did not abolish this serotonin-induced release of catecholamines. The serotonin-induced release of adrenaline, however, was abolished totally by the addition of methysergide. Serotonin is present in high concentrations (44.61+/−5.96 microgram g-1 tissue) in the anterior region of the posterior cardinal vein within the head kidney. Carbachol (10–5 mol kg-1) did not elicit release of the stored serotonin from the perfused head kidney preparation. We conclude that the chromaffin cells in the perfused trout head kidney preparation display characteristics similar to those of other vertebrates and that this preparation is a useful tool for studying the control of catecholamine release in fish. The results demonstrate that serotonin has a direct impact on the chromaffin cells by interacting with methysergide-sensitive receptors to initiate the release of adrenaline. The potential physiological role of serotonin on catecholamine release in trout is discussed.
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Maggs, D. G., and I. A. Macdonald. "Physiological and Symptomatic Responses to Postural Change in Non-Diabetic Subjects during Hypoglycaemia." Clinical Science 87, no. 2 (August 1, 1994): 193–99. http://dx.doi.org/10.1042/cs0870193.
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1. Insulin-induced hypoglycaemia is characterized by an autonomic disturbance which produces some of the symptoms of hypoglycaemia. How an additional autonomic stress like postural change may alter physiological responses and symptoms of hypoglycaemia is not known. In 10 healthy male subjects (mean age 24 years) we observed physiological and symptomatic responses to postural change during acute (20 min) and prolonged (60 min) hyperinsulinaemic (60 m-units min−1 m−2) hypoglycaemia (2.5 mmol/l) and euglycaemia (4.5 mmol/l), and placebo control (saline). 2. In all studies standing increased plasma catecholamines (adrenaline, P < 0.001; noradrenaline, P < 0.0001), blood pressure (P < 0.0001) and heart rate (P < 0.0001). Catecholamine responses to standing were augmented by acute hypoglycaemia (adrenaline, P < 0.005; noradrenaline, P < 0.01), but less so by prolonged hypoglycaemia (adrenaline, P < 0.05; noradrenaline, P < 0.05). Supine heart rate was higher before standing during prolonged hypoglycaemia (P < 0.05), but did not increase as much on standing when compared with acute hypoglycaemia and prolonged euglycaemia. 3. During acute hypoglycaemia, autonomic symptoms increased on standing, but during prolonged hypoglycaemia, in the presence of generally higher symptom scores, standing had no effect. Autonomic symptoms, with the exception of hunger, tended to decrease with time (P < 0.05) during prolonged hypoglycaemia. 4. To conclude, posture does modify the catecholamine and symptomatic responses to hypoglycaemia, but this effect is dependent on the duration of hypoglycaemia. Hypoglycaemia and hyperinsulinaemia had little or no effect on the cardiovascular responses to changing posture.
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Mader, S. L., C. L. Downing, and E. Van Lunteren. "Effect of age and hypoxia on beta-adrenergic receptors in rat heart." Journal of Applied Physiology 71, no. 6 (December 1, 1991): 2094–98. http://dx.doi.org/10.1152/jappl.1991.71.6.2094.
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Previous reports suggest that hypoxia downregulates cardiac beta-adrenergic receptors from young rats. Because aging alters response to stress, we hypothesized an age-related alteration in the response to hypoxia. Male Fischer-344 rats, aged 3 and 20 mo, were divided into control and hypoxic groups. The hypoxic rats were exposed to hypobaric hypoxia (0.5 atm) for 3 wk. After hypoxic exposure, body weight decreased, hematocrit increased, right ventricular weight increased, and left ventricular weight decreased in all animals. beta-Adrenergic receptor density declined after hypoxic exposure in the young but not in the older animals, a change that was confined to the left ventricle. beta-Adrenergic receptor density in the right ventricle was significantly lower in the older animals than in the young animals. Plasma catecholamines (norepinephrine, epinephrine) drawn after the animals were killed (stress levels) decreased in young rats and increased in old rats after the exposure to hypoxia. Hypoxia is a useful physiological stress that elucidates age-related changes in cardiac beta-adrenergic receptor and catecholamine regulation that have not previously been described.
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Pinz, Ilka, and Hans-O. Pörtner. "Metabolic costs induced by lactate in the toad Bufo marinus: new mechanism behind oxygen debt?" Journal of Applied Physiology 94, no. 3 (March 1, 2003): 1177–85. http://dx.doi.org/10.1152/japplphysiol.00131.2002.
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The mechanism of an increase in metabolic rate induced by lactate was investigated in the toad Bufo marinus. Oxygen consumption (V˙o 2) was analyzed in fully aerobic animals under hypoxic conditions (7% O2 in air), accompanied by measurements of catecholamines in the plasma, and was measured in isolated hepatocytes in vitro under normoxia by using specific inhibitors of lactate proton symport [α-cyano-4-hydroxycinnamate (CHC)] and sodium proton exchange (EIPA). The rise in metabolic rate in vivo can be elicited by infusions of hyperosmotic (previous findings) or isosmotic sodium lactate solutions (this study). Despite previous findings of reduced metabolic stimulation under the effect of adrenergic blockers, the increase inV˙o 2 in vivo was not associated with elevated plasma catecholamine levels, suggesting local release and effect. In addition to the possible in vivo effect via catecholamines, lactate induced a rise in V˙o 2 of isolated hepatocytes, depending on the concentration present in a weakly buffered Ringer solution at pH 7.0. No increase was found at higher pH values (7.4 or 7.8) or in HEPES-buffered Ringer solution. Inhibition of the Lac−-H+ transporter with α-CHC or of the Na+/H+ exchanger with EIPA prevented the increase in metabolic rate. We conclude that increasedV˙o 2 at an elevated systemic lactate level may involve catecholamine action, but it is also caused by an increased energy demand of cellular acid-base regulation via stimulation of Na+/H+ exchange and thereby Na+-K+-ATPase. The effect depends on entry of lactic acid into the cells via lactate proton symport, which is likely favored by low cellular surface pH. We suggest that these energetic costs should also be considered in other physiological phenomena, e.g., when lactate is present during excess, postexerciseV˙o 2.
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Myburgh, J. A., R. N. Upton, C. Grant, and A. Martinez. "The Cerebrovascular Effects of Adrenaline, Noradrenaline and Dopamine Infusions under Propofol and Isoflurane Anaesthesia in Sheep." Anaesthesia and Intensive Care 30, no. 6 (December 2002): 725–33. http://dx.doi.org/10.1177/0310057x0203000602.
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Infusions of catecholamines are frequently administered to patients receiving propofol or isoflurane anaesthesia. Interactions between these drugs may affect regional circulations, such as the brain. The aim of this animal (sheep) study was to determine the effects of ramped infusions of adrenaline, noradrenaline (10, 20, 40 μg/min) and dopamine (10, 20, 40 μg/kg/min) on cerebral blood flow (CBF), intracranial pressure (ICP), cerebrovascular resistance (CVR) and cerebral metabolic rate for oxygen (CMRO 2 ). These measurements were made under awake physiological conditions, and during continuous propofol (15 mg/min) or 2% isoflurane anaesthesia. All three catecholamines significantly and equivalently increased mean arterial pressure from baseline in a dose-dependent manner in the three cohorts (P<0.001). In the awake cohort (n=8), dopamine (P<0.01) significantly increased CBF from baseline whilst adrenaline and noradrenaline did not (P> 0.05). Under propofol (n=6) and isoflurane (n=6), all three catecholamines significantly increased CBF (P<0.001). Dopamine caused the greatest increase in CBF, and was associated with significant increases in ICP (awake: P<0.001; propofol P<0.05; isoflurane P<0.001) and CVR (isoflurane P<0.05). No significant changes in CMRO 2 were demonstrated. Under propofol and isoflurane anaesthesia, the cerebrovascular effects of catecholamines were significantly different from the awake, physiological state, with dopamine demonstrating the most pronounced effects, particularly under propofol. Dopamine-induced hyperaemia was associated with other cerebrovascular changes. In the presence of an equivalent effect on mean arterial pressure, the exaggerated cerebrovascular effects under anaesthesia appear to be centrally mediated, possibly induced by propofol- or isoflurane-dependent changes in blood-brain barrier permeability, thereby causing a direct influence on the cerebral vasculature.
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Ekpe, E. D., J. A. Moibi, and R. J. Christopherson. "Beta-adrenergic receptors in skeletal muscles of ruminants: Effects of temperature and feed intake." Canadian Journal of Animal Science 80, no. 1 (March 1, 2000): 79–86. http://dx.doi.org/10.4141/a99-027.
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Adrenergic receptors mediate effects of catecholamines on physiological processes including protein and energy metabolism. We determined the effects of temperature and feed intake on beta-1 and beta-2 adrenergic receptors (β1 AR and β2 AR) in skeletal muscle of lambs to assess the potential to modify physiological responses through adrenergic receptors. Twenty-four wether lambs received either restricted (R) or ad libitum (A) levels of feed intake, and were exposed to either cold (C; 0 ± 2 °C) or warm (W; 23 ± 2 °C) temperatures, resulting in four experimental treatment groups (WA, WR, CA and CR). At the end of 4 mo the lambs were slaughtered and biceps femoris, semitendinosus and gastrocnemius muscles were harvested for isolation of plasma membrane. Binding of [3H]dihydroalprenolol to crude plasma membrane was used to determine the β AR densities and binding affinities (Kd). The densities of β1 AR were 28.02 ± 4.17, 40.68 ± 2.26, 28.99 ± 4.68 and 55.56 ± 6.05 fmol mg−1 protein for biceps femoris, 29.35 ± 1.49, 35.34 ± 2.59, 28.36 ± 2.94 and 37.89 ± 3.30 fmol mg−1 protein for gastrocnemius, and 22.66 ± 2.66, 31.21 ± 4.65, 21.84 ± 1.81 and 38.62 ± 3.67 fmol mg−1 protein for semitendinosus, for WA, WR, CA and CR, respectively. The Kd values for all groups ranged from 1.7 to 8.5 nM for β1 AR. Feed restriction increased (P < 0.01) the density of β1 AR in both environments but there was no significant effect of temperature. β1 AR densities and binding affinities were significantly higher in biceps femoris than in gastrocnemius and semitendinosus muscles when feed intake was restricted. The densities of β2 AR ranged from 9.0 to 16.0 fmol mg−1 protein. There was no effect of treatments on the density or receptor binding affinity of β2 AR in muscles. It is concluded that feed restriction causes increased density of β1 AR in sheep and that feed restriction could potentially increase the metabolic responsiveness of skeletal muscle to elevated levels of catecholamines. Key words: Catecholamine receptors, skeletal muscle, temperature, feed
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Crowe, Melissa J., Anthony S. Leicht, and Warwick L. Spinks. "Physiological and Cognitive Responses to Caffeine during Repeated, High-Intensity Exercise." International Journal of Sport Nutrition and Exercise Metabolism 16, no. 5 (October 2006): 528–44. http://dx.doi.org/10.1123/ijsnem.16.5.528.
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This study investigated the effects of caffeine on repeated, anaerobic exercise using a double-blind, randomized, crossover design. Seventeen subjects (five female) underwent cognitive (reaction time, number recall) and blood (glucose, potassium, catecholamines, lactate) testing before and after consuming caffeine (6 mg/kg), placebo, or nothing (control). An exercise test (two 60 s maximal cycling bouts) was conducted 90 min after caffeine/placebo consumption. Plasma caffeine concentrations significantly increased after caffeine ingestion, however, there were no positive effects on cognitive or blood parameters except a significant decrease in plasma potassium concentrations at rest. Potentially negative effects of caffeine included significantly higher blood lactate compared to control and significantly slower time to peak power in exercise bout 2 compared to control and placebo. Caffeine had no significant effect on peak power, work output, RPE, or peak heart rate. In conclusion, caffeine had no ergogenic effect on repeated, maximal cycling bouts and may be detrimental to anaerobic performance.
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Petrov, N. A., S. N. Zorin, N. A. Biryulina, and V. K. Mazo. "Physiological and Biochemical Evaluation of the Effectiveness of a New Food Ingredient, a Source of Phytoecdysteroids and Flavonoids from Quinoa Grain." Biotekhnologiya 37, no. 5 (2021): 88–95. http://dx.doi.org/10.21519/0234-2758-2021-37-5-88-95.
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Abstract- One of the promising food sources of biologically active substances is quinoa grain, which is valued for its high content of protein, sulfur-containing amino acids, lysine, fiber, and minerals. In addition, quinoa grain can be a valuable food source of polyphenolic compounds and phytoecdysteroids. The method for production of a concentrate of flavonoids and 20-hydroxyecdysone from quinoa grains sorbed on coagulated egg protein has been developed. The in vivo evaluation of efficacy of the developed food ingredient was conducted using male Wistar rats under immobilization stress and after exhausting physical exertion. The consumption of the food ingredient prevented an increase in the level of the main stress markers, catecholamines, in animals subjected to immobilization stress. The opposite effect was observed in animals that received the food ingredient after exhausting physical exertion: their levels of catecholamines were significantly higher than in the rest comparison groups. Using the Elevated Plus Maze and Open Field tests, it was shown that the consumption of the developed concentrate neutralized the negative effect of immobilization stress and treadmill exercise on anxiety in Wistar rats. The results obtained require additional study under conditions of preventive introduction of the food ingredient into the diet of intact animals, as well as a toxicological safety assessment. Key words: quinoa, 20-hydroxyecdysone, flavonoids, stress, immobilization, exhaustive physical exercise, catecholamines, corticosterone This work was supported by the Russian Scientific Foundation, grant no. 19-16-00107.
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Oyama, K., J. Padbury, B. Chappell, A. Martinez, H. Stein, and J. Humme. "Single umbilical artery ligation-induced fetal growth retardation: effect on postnatal adaptation." American Journal of Physiology-Endocrinology and Metabolism 263, no. 3 (September 1, 1992): E575—E583. http://dx.doi.org/10.1152/ajpendo.1992.263.3.e575.
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To assess whether prolonged intrauterine stress and resultant fetal growth retardation result in depletion of adrenal catecholamines and alter the adrenergic signal transduction system, we studied newborn sheep after single umbilical artery ligation (SUAL)-induced growth retardation. The animals were delivered at term, and postnatal cardiovascular, pulmonary, endocrine, and metabolic responses were measured. We also evaluated the status of myocardial and pulmonary beta-adrenergic receptor number and function. SUAL caused significant growth retardation but relative preservation of brain and adrenal gland weight and adrenal catecholamine content. Blood pressure, plasma free fatty acid, and glucose responses at birth were blunted in SUAL animals. The plasma epinephrine (Epi) and norepinephrine levels were comparable in both groups for the first 2 h of age. By 4 h, both plasma concentration and plasma appearance rate of Epi were reduced to 40% of control in SUAL animals (P less than 0.05). Neither beta-receptor density, affinity, nor adenylate cyclase activity were altered by SUAL in either cardiac or pulmonary membranes. These results suggest that, rather than overt depletion, there is relative sparing of initial adrenal medullary function that later waned. This response and preservation of the beta-adrenergic signal transduction system may represent partial compensation for the physiological stress induced by SUAL.
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Rochon, L., and L. J. Bukowiecki. "Alterations in adipocyte response to lipolytic hormones during cold acclimation." American Journal of Physiology-Cell Physiology 258, no. 5 (May 1, 1990): C835—C840. http://dx.doi.org/10.1152/ajpcell.1990.258.5.c835.
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The effects of cold exposure (7 days, 5 degrees C) and cold acclimation (21 days, 5 degrees C) on the regulation of lipolysis were investigated in adipocytes isolated from epididymal fat pads of rats. Catecholamines stimulated lipolysis in an affinity sequence typical of the beta 1-adrenoceptor subtype: one-half maximum velocity (1/2 Vmax) isoproterenol (35 nM) much greater than 1/2 Vmax norepinephrine (150 nM) approximately 1/2 Vmax epinephrine (200 nM). Cold exposure markedly decreased the sensitivity (1/2 Vmax) and the responsiveness (Vmax) of the adipocytes to the lipolytic action of catecholamines. Addition of adenosine deaminase to fat cells isolated from cold-exposed rats did not normalize the lipolytic activity, suggesting that extracellular adenosine was not responsible for the obtunded lipolysis. This effect of cold exposure was transient as the lipolytic response to catecholamines was normal in fully cold-acclimated animals. Remarkably, the responsiveness of adipocytes to the lipolytic action of glucagon (200 nM) and adrenocorticotropic hormone (ACTH, 1 microM) progressively increased during cold acclimation. Adipocyte lipolytic response to dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) and theophylline was normal in cold-exposed rats, indicating that the lipolytic defect resides at an early step in the lipolytic cascade (pre-cAMP). On the other hand, the antilipolytic effect of insulin on norepinephrine-induced lipolysis significantly decreased during cold acclimation, particularly at physiological levels of insulin (nanomolar level). These results demonstrate that the transient decrease in the lipolytic action of catecholamines observed during cold acclimation is compensated by 1) an increased responsiveness of adipocytes to glucagon and ACTH and 2) by a decreased effectiveness of insulin to induce antilipolysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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Myers, L. M., and C. Sumners. "Regulation of angiotensin II binding sites in neuronal cultures by catecholamines." American Journal of Physiology-Cell Physiology 257, no. 4 (October 1, 1989): C706—C713. http://dx.doi.org/10.1152/ajpcell.1989.257.4.c706.
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Previous studies determined that direct activation of protein kinase C (PKC) with phorbol esters increases the number of angiotensin II (ANG II)-specific binding sites in neuronal cultures prepared from the hypothalamus and brain stem of 1-day-old rats. In the physiological situation, PKC is activated by diacylglycerol, which can be produced by multiple pathways, such as stimulation of inositol phospholipid (IP) hydrolysis, phosphatidylcholine hydrolysis, or by de novo synthesis. In the present study we have examined whether stimulation of IP hydrolysis, and presumably activation of PKC, can mimic the actions of phorbol esters on ANG II-specific binding. We have incubated neuronal cultures with agents that increase IP hydrolysis and have determined the effects on ANG II-specific binding. Incubation of neuronal cultures with norepinephrine (NE) at concentrations (greater than 5 microM) and for times (15-60 min) that cause large increases in IP hydrolysis caused increases in the number of ANG II-specific binding sites, mimicking the actions of phorbol esters. The return of IP hydrolysis to control values was associated with a return of ANG II-specific binding to control levels. The upregulatory action of NE was abolished by prazosin, demonstrating the involvement of alpha 1-adrenergic receptors. In addition, this effect was blunted by the PKC antagonist H 7, suggesting PKC involvement in the response. Thus we have determined a potential physiological mechanism by which stimulation of IP hydrolysis by NE, and possible subsequent activation of PKC, leads to upregulation of ANG II-specific binding sites in neuronal cultures.(ABSTRACT TRUNCATED AT 250 WORDS)
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Massé, Chantal, and Yves Berthiaume. "Effect of adrenalectomy on pulmonary edema resolution." Clinical and Investigative Medicine 42, no. 2 (June 23, 2019): E33–37. http://dx.doi.org/10.25011/cim.v42i2.32814.
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Purpose: The capacity of the lung to clear edema fluid has been shown to be one of the factors that can influence the prognosis of cardiogenic and noncardiogenic pulmonary edema. Active Na+ transport across the alveolar epithelium is the main driving force involved in this physiological process. Since endogenous catecholamines are known to activate the sodium-dependent mechanism of alveolar edema clearance, the objective of the present study was to explore if adrenalectomy, which prevents the release of endogenous catecholamines and other hormones, such as corticosterone, into circulation, would affect edema resolution in a model of lung injury induced by thiourea.
Methods: A high-permeability pulmonary edema was induced in adult male Sprague-Dawley rats using a thiourea-induced pulmonary edema model. To determine if the release of adrenalin and corticosterone is essential for resolution of the thiourea-induced edema, we measured 1) the release of adrenalin and corticosterone in urine and 2) edema resolution in control animals and adrenalectomized animals.
Results: The administration of thiourea significantly increased the wet-to-dry ratio after four and eight hours. After 12 and 24 hours, the wet-to-dry ratio gradually returned to baseline. Although thiourea-induced pulmonary edema was associated with a significant increase in urine adrenalin and corticosterone, the absence of adrenalin and corticosterone response in adrenalectomized animals did not prevent the resolution of the edema.
Conclusions: These experiments demonstrated that resolution of thioureainduced pulmonary edema can occur in the absence of hormonal secretion by the adrenal glands.
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Syuu, Yi, Hiromi Matsubara, Shingo Hosogi, and Hiroyuki Suga. "Pressor effect of electroacupuncture on hemorrhagic hypotension." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, no. 6 (December 2003): R1446—R1452. http://dx.doi.org/10.1152/ajpregu.00243.2003.
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Neiguan (PC-6) is a traditional acupoint in each forearm and overlies the trunk of the median nerve. Previous studies show that electroacupuncture (EA) at the Neiguan acupoint could improve not only myocardial ischemic dysfunction by inducing a depressor response but also recover hemorrhagic hypotension by inducing a pressor response. However, their physiological mechanisms are not yet elucidated. We investigated the pressor effect of Neiguan EA and its mechanism by focusing on left ventricular (LV) performance in a canine hemorrhagic hypotension model. We hemorrhaged 36 anesthetized and thoracotomized mongrel dogs and decreased LV end-systolic pressure (ESP) to ∼70 mmHg (35% decrease). We obtained LV pressure-volume (P-V) data with a micromanometer catheter and a conductance catheter. One-hour Neiguan EA significantly recovered the decreased ESP, end-diastolic volume, and stroke volume by 32 ± 13%, 27 ± 13%, and 39 ± 17%, respectively ( P < 0.05), without changing heart rate and the slope of the end-systolic P-V relation. Neiguan EA inhibited a hemorrhage-induced increase in plasma catecholamines. However, vecuronium (neuromuscular blocking agent) administration abolished the antihypotension effect of Neiguan EA. Furthermore, Neiguan EA was much more effective than a nonacupoint thigh EA. We conclude that Neiguan EA achieved the antihypotension effect by improving LV filling of the hemorrhage-depressed LV performance despite the inhibition of the hemorrhage-increased plasma catecholamines. This pressor effect seemed to accompany an increased venous return by Neiguan EA-increased vasomotor tone and muscle pump. This study demonstrated a scientific basis for the therapeutic efficacy of acupuncture in the treatment of hemorrhagic hypotension and shock.
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Gross, R., and P. Mialhe. "Glucose, β adrenergic effects, and pancreatic endocrine function in the isolated perfused duck pancreas." Acta Endocrinologica 115, no. 1 (May 1987): 105–11. http://dx.doi.org/10.1530/acta.0.1150105.
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Abstract. Duck isolated perfused pancreas was used to assess glucose, adrenergic mediated effects and pancreatic function interrelationships. A moderate physiological 50% increase in glucose level, corresponding closely to the difference observed between 24-h-fasted and fed animals, induced a significant decrease of pancreatic glucagon not due to a rise in somatostatin secretion. The great responsiveness of the A cell was still found after glucagon stimulation by catecholamines or β adrenergic agonism. Insulin was irresponsive to the glucose load we used, suggesting that glucose-induced glucagon suppression was also insulin independent. As far as the D cell was concerned, glucose had no effect on pancreatic somatostatin output; however, an interesting finding was that β adrenergic agonism has a permissive effect on D cell responsiveness to the nutriment.
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Primmett, D. R., D. J. Randall, M. Mazeaud, and R. G. Boutilier. "The role of catecholamines in erythrocyte pH regulation and oxygen transport in rainbow trout (Salmo gairdneri) during exercise." Journal of Experimental Biology 122, no. 1 (May 1, 1986): 139–48. http://dx.doi.org/10.1242/jeb.122.1.139.
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Rainbow trout were subjected to burst swimming to exhaustion followed by 4 h aerobic swimming at 80% critical swimming velocity. Severe physiological disturbances, including a marked plasma acidosis caused by the burst swim, were corrected during the 4 h of subsequent aerobic exercise. Erythrocytic pH and arterial oxygen content increased, even though plasma pH was reduced. We suggest that the increase in erythrocytic pH was caused by the action of elevated adrenaline and noradrenaline levels in the blood acting on beta-adrenergic receptors on the trout red blood cell, causing the cell to swell and raising intracellular pH, offsetting any effect of a reduction of plasma pH on erythrocyte pH and haemoglobin-oxygen binding. Propranolol blocked the action of catecholamines on trout erythrocytes. We conclude that catecholamines play an important role in maintaining oxygen transport to aerobic muscles, following burst swimming and the associated acidotic conditions.
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Zhang, Lian, Fangwen Rao, Jennifer Wessel, Brian P. Kennedy, Brinda K. Rana, Laurent Taupenot, Elizabeth O. Lillie, et al. "Functional allelic heterogeneity and pleiotropy of a repeat polymorphism in tyrosine hydroxylase: prediction of catecholamines and response to stress in twins." Physiological Genomics 19, no. 3 (November 17, 2004): 277–91. http://dx.doi.org/10.1152/physiolgenomics.00151.2004.
Full textAbstract:
Tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis, has a common tetranucleotide repeat polymorphism, (TCAT) n. We asked whether variation at (TCAT) n may influence the autonomic nervous system and its response to environmental stress. To understand the role of heredity in such traits, we turned to a human twin study design. Both biochemical and physiological autonomic traits displayed substantial heritability (h2), up to h2 = 56.8 ± 7.5% ( P < 0.0001) for norepinephrine secretion, and h2 = 61 ± 6% ( P < 0.001) for heart rate. Common (TCAT) n alleles, particularly (TCAT)6 and (TCAT)10i, predicted such traits (including catecholamine secretion, as well as basal and poststress heart rate) in allele copy number dose-dependent fashion, although in directionally opposite ways, indicating functional allelic heterogeneity. (TCAT) n diploid genotypes (e.g., [TCAT]6/[TCAT]10i) predicted the same physiological traits but with increased explanatory power for trait variation (in contrast to allele copy number). Multivariate ANOVA documented genetic pleiotropy: joint effects of the (TCAT)10i allele on both biochemical (norepinephrine) and physiological (heart rate) traits. (TCAT)6 allele frequencies were lower in normotensive twins at genetic risk of hypertension, consistent with an effect to protect against later development of hypertension, and suggesting that the traits predicted by these variants in still-normotensive subjects are early, heritable, “intermediate phenotypes” in the pathogenetic scheme for later development of sustained hypertension. We conclude that common allelic variation within the tyrosine hydroxylase locus exerts a powerful, heritable effect on autonomic control of the circulation and that such variation may have implications in later development of cardiovascular disease traits such as hypertension.
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Kolesnikova, L. R., O. A. Makarova, L. V. Natyaganova, M. I. Dolgikh, and L. I. Korytov. "Metabolism and Physiological Functions Adjustment of the Organism under Stress Influence." Acta Biomedica Scientifica 3, no. 6 (January 5, 2019): 15–22. http://dx.doi.org/10.29413/abs.2018-3.6.2.
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Stress reaction of the organism is a process occurring at the cellular, tissue and systemic levels. The organism responds to any adverse effect with a multi-level reaction, which causes the development of stress and, as a result, adaptation. The damaging effect is due to the excessive strengthening of another adaptive effect – lipotropic, that increases the activity of phospholipases and the intensity of free radical oxidation of lipids through the catecholamines and protein kinases. The changes in the immune system during the adaptation stage are to maintain antigenic homeostasis of the internal environment of the organism due to lymphoid cells, lymphocytes and cytokines. Almost all cells with antigen representation function are capable to produce interleukins under certain conditions. The vascular system is a kind of an indicator of any pathological process, determining the state of regulatory and adaptive mechanisms, the features of the connective tissue matrix. Stress causes a restructuring of metabolism and physiological functions, which increases the organism’s resistance to acute death. Thus, the physiological meaning of the stress reaction is the emergency mobilization of energy and structural resources of the organism and the creation of positive background for the implementation of reactions, aimed at maintaining homeostasis in extreme situations.
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KANIA, BOGDAN FELIKS, DANUTA WROŃSKA, IZABELA SZPRĘGIEL, and URSZULA BRACHA. "Glutamate as a neural factor for the ex vivo release of catecholamines from the rabbit hippocampus." Medycyna Weterynaryjna 78, no. 06 (2022): 6670–2022. http://dx.doi.org/10.21521/mw.6670.
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The aim of the research was to confirm the hypothesis about the direct influence of different concentrations of glutamate (Glu; 5, 50 and 200 μM) on the release of catecholamines (CA’s) from hippocampal slices incubated for 90 min. The hippocampus is the central structure of the motivational system and, along with the hypothalamus, amygdala, and medial prefrontal cortex (mPFC), is responsible for memory, learning, and the initiation and course of the reaction to stressoric factors. In our research, we focused on the direct effect of different Glu concentrations on CA release without the involvement of other neural cerebral structures and humoral responses. The effect of Glu added to the incubation fluid was found to be inconsistent. When added at the lowest concentration, Glu inhibited the release of CA from the incubated slices, and at higher concentrations tended to increase the release of CA. Notably, Glu significantly increased the release of epinephrine (E) from incubated slices of the hippocampus. These effects may suggest that physiological concentrations of Glu inhibit CA release from hippocampal neurons in vitro and therefore enhance its excitatory effects in vivo.
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Nishikiori, M., K. Takenaka, T. Endo, Y. Monma, K. Ueno, M. Minami, N. Yamazaki, M. Matsumoto, H. Saito, and S. Takeo. "Physiological role of sulfate conjugation of catecholamines: positive inotropic effect of sulfate conjugated dopamine in guinea-pig atria." European Journal of Pharmacology 183, no. 2 (July 1990): 349–50. http://dx.doi.org/10.1016/0014-2999(90)93216-d.
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Galitzky, J., M. Reverte, M. Portillo, C. Carpene, M. Lafontan, and M. Berlan. "Coexistence of beta 1-, beta 2-, and beta 3-adrenoceptors in dog fat cells and their differential activation by catecholamines." American Journal of Physiology-Endocrinology and Metabolism 264, no. 3 (March 1, 1993): E403—E412. http://dx.doi.org/10.1152/ajpendo.1993.264.3.e403.
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The existence of a beta 3-adrenoceptor (in addition to classical beta 1- and beta 2-), its involvement in the control of lipolysis and its recruitment by catecholamines were investigated in dog adipose tissue. Isoproterenol, norepinephrine, and the beta 2-selective agonist procaterol fully activated lipolysis in adipocytes (order of potency: isoproterenol > norepinephrine = procaterol). beta 3-Adrenergic agonists stimulated lipolysis with the order of potency: BRL 37344 > CGP 12177 > SR 58611A. Propranolol and bupranolol (nonselective beta-antagonists) antagonized, with a low potency, the effect of BRL 37344, whereas the beta 1-antagonist CGP 20712A and the beta 2-antagonist ICI 118551 were without action. CGP 20712A inhibited the effect of lower concentrations of agonists (0.05 microM isoproterenol, 0.1 microM norepinephrine and 0.1 microM procaterol) with an inhibitory constant (mean Ki) of 0.0075, 0.032 and > 10 microM, respectively. Mean Ki values for the beta 2-antagonist ICI 118551 were 1.744, 1.243, and 0.019 microM. This result indicates that low concentrations of isoproterenol and norepinephrine stimulate lipolysis mainly via beta 1-adrenoceptors in dog fat cells. Inversely, the lipolytic effect of higher concentrations of agonists i.e., 1 microM isoproterenol and catecholamines, was weakly antagonized by CGP 20712A or ICI 118551 while the nonselective beta-antagonists bupranolol and propranolol suppressed the effects with the order of potency expected for a beta 3-adrenoceptor: bupranolol > propranolol. These data indicate 1) the presence of a functional beta 3-adrenoceptor that coexists with beta 1- and beta 2-adrenoceptors in dog fat cells; 2) a separation of the differential potencies of physiological amines in the activation of lipolysis through beta 1-, beta 2-, and beta 3-adrenoceptors; the lipolytic response initiated at low concentrations (submicromolar range) of norepinephrine is primarily mediated by the beta 1-adrenoceptor subtype; and 3) an activation of the beta 3-adrenoceptor that occurs at higher concentrations of catecholamines.
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Lowe, Tim E., Neville G. Gregory, Andrew D. Fisher, and Steven R. Payne. "The effects of temperature elevation and water deprivation on lamb physiology, welfare, and meat quality." Australian Journal of Agricultural Research 53, no. 6 (2002): 707. http://dx.doi.org/10.1071/ar01125.
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Romney-cross ewe lambs (n = 27) were subjected to controlled environmental conditions to induce acute heat stress. The goals of the study were to: (1) determine appropriate physiological indicators of acute heat stress, (2) determine threshold rectal temperatures (Tr) for catecholamine and cortisol release, (3) determine effects on meat quality, and (4) assess the effect of dehydration on the above measures. There were 3 treatments: control (ambient temperature and humidity), heat stress (33°C, and 85-100% humidity), and heat stress combined with water deprivation. The duration of the treatment period was 12 h. Respiration rate (Rf) and rectal temperature (Tr) were highly correlated with increasing temperature humidity index (THI) (r > 0.75, P < 0.001), whereas heart rate was less responsive to THI (r = 0.30, P < 0.05). The welfare of these lambs was at risk at Tr greater than 40.5°C, a point at which respiration rate was maximal and unable to prevent further increases in Tr. Plasma cortisol concentrations were increased in heat-stressed lambs after Tr reached approximately 40.7°C. Plasma catecholamines were only elevated in lambs when Tr was greater than 42°C. The majority of lambs subjected to heat stress had a Tr less than 42°C, and there were no significant effects on meat quality. Despite exhibiting increases in plasma protein concentrations, there were no indications that dehydrated lambs were under additional stress during heat challenge in comparison with hydrated lambs.
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Landry, Jean-François, Jean-Pierre Després, Denis Prud'homme, Benoît Lamarche, Angelo Tremblay, André Nadeau, and Claude Bouchard. "A study of some potential correlates of the hypotensive effects of prolonged submaximal exercise in normotensive men." Canadian Journal of Physiology and Pharmacology 70, no. 1 (January 1, 1992): 53–59. http://dx.doi.org/10.1139/y92-008.
Full textAbstract:
This study was undertaken (1) to examine the relation of plasma catecholamine and insulin levels to the blood pressure response during and after submaximal exercise, (2) to verify whether the blood pressure response to an epinephrine infusion is associated with the blood pressure response to a prolonged submaximal exercise, and (3) to study some potential correlates of the hypotensive effect of prolonged aerobic exercise. Nine normotensive young men (mean age 22.0 ± 1.4 years) were subjected to a 1-h epinephrine infusion protocol and a 1-h submaximal exercise test on a cycle ergometer. The two tests were performed 1 week apart. The physiological and hormonal responses observed during the submaximal exercise test were generally greater than those observed during the epinephrine infusion test. Blood pressure responses in both tests showed no significant association with changes in plasma insulin levels. Changes in plasma norepinephrine concentration were positively correlated with changes in systolic blood pressure during the submaximal exercise test but not during the epinephrine infusion. Results also showed that the blood pressure response to epinephrine infusion was not correlated with the blood pressure response to submaximal exercise. However, post-exercise and post-infusion systolic blood pressure responses (differences between "post-test" and "resting" values) were significantly associated (r = 0.81, p < 0.01). In addition, a significant hypotensive effect of submaximal exercise was observed for both systolic and diastolic blood pressure. However, the individual differences observed in the hypotensive effect of aerobic exercise appeared to be more related to variations in vascular sensitivity than to exercise-induced variations in plasma insulin and catecholamine levels, at least in this sample of healthy normotensive young men.Key words: blood pressure, exercise, catecholamines, insulin, epinephrine infusion.
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Vranic, Mladen. "Odyssey between Scylla and Charybdis through storms of carbohydrate metabolism and diabetes: a career retrospective." American Journal of Physiology-Endocrinology and Metabolism 299, no. 6 (December 2010): E849—E867. http://dx.doi.org/10.1152/ajpendo.00344.2010.
Full textAbstract:
This research perspective allows me to summarize some of my work completed over 50 years, and it is organized in seven sections. 1) The treatment of diabetes concentrates on the liver and/or the periphery. We quantified hormonal and metabolic interactions involved in physiology and the pathogenesis of diabetes by developing tracer methods to separate the effects of diabetes on both. We collaborated in the first tracer clinical studies on insulin resistance, hypertriglyceridemia, and the Cori cycle. 2) Diabetes reflects insulin deficiency and glucagon abundance. Extrapancreatic glucagon changed the prevailing dogma and permitted precise exploration of the roles of insulin and glucagon in physiology and diabetes. 3) We established the critical role of glucagon-insulin interaction and the control of glucose metabolism during moderate exercise and of catecholamines during strenuous exercise. Deficiencies of the release and effects of these hormones were quantified in diabetes. We also revealed how acute and chronic hyperglycemia affects the expression of GLUT2 gene and protein in diabetes. 4) We outlined molecular and physiological mechanisms whereby exercise training and repetitive neurogenic stress can prevent diabetes in ZDF rats. 5) We and others established that the indirect effect of insulin plays an important role in the regulation of glucose production in dogs. We confirmed this effect in humans and demonstrated that in type 2 diabetes it is mainly the indirect effect. 6) We indicated that the muscle and the liver protected against glucose changes. 7) We described molecular mechanisms responsible for increased HPA axis in diabetes and for the diminished responses of HPA axis, catecholamines, and glucagon to hypoglycemia. We proposed a new approach to decrease the threat of hypoglycemia.
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Rubanyi, G. M., R. R. Lorenz, and P. M. Vanhoutte. "Bioassay of endothelium-derived relaxing factor(s): inactivation by catecholamines." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 1 (July 1, 1985): H95—H101. http://dx.doi.org/10.1152/ajpheart.1985.249.1.h95.
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A bioassay technique was developed to analyze the effect of vasoactive substance(s) released from endothelial cells. Canine femoral arteries with or without endothelium were perfused with physiological salt solution at 37 degrees C. The perfusate was bioassayed with a ring of coronary artery without endothelium. A substance(s) released by the endothelial cells under basal conditions caused relaxation of unstimulated coronary arteries or relaxation of those contracted with prostaglandin F2 alpha. The release of the relaxing substance(s) was augmented by acetylcholine. The relaxation induced by acetylcholine was biphasic: an initial rapid phase followed by a partial recovery and a slowly developing prolonged relaxation; the half-life of the substance(s) causing the initial phase averaged 6.3 s. Norepinephrine, epinephrine, and ascorbic acid, given downstream of the femoral artery, reversibly prevented the second phase but only attenuated the initial relaxation. These observations indicate that an endothelium-derived relaxing substance(s) is released into the lumen of the femoral artery under basal conditions and during stimulation with acetylcholine. Catecholamines can inactivate the relaxing substance(s) but do not prevent either its production by endothelial cells or its action on vascular smooth muscle.
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Hilsted, J., N. J. Christensen, and S. Larsen. "Effect of Catecholamines and Insulin on Plasma Volume and Intravascular Mass of Albumin in Man." Clinical Science 77, no. 2 (August 1, 1989): 149–55. http://dx.doi.org/10.1042/cs0770149.
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1. The effect of intravenous catecholamine infusions and of intravenous insulin on plasma volume and intravascular mass of albumin was investigated in healthy males. 2. Physiological doses of adrenaline (0.5 μg/min and 3 μg/min) increased peripheral venous packed cell volume significantly; intravenous noradrenaline at 0.5 μg/min had no effect on packed cell volume, whereas packed cell volume increased significantly at 3 μg of noradrenaline/min. No significant change in packed cell volume was found during saline infusion. 3. During adrenaline infusion at 6 μg/min, packed cell volume increased, plasma volume decreased and intravascular mass of albumin decreased significantly. During noradrenaline infusion at 6 μg/min, packed cell volume increased and plasma volume decreased, but intravascular mass of albumin did not change. 4. Application of a hyperinsulinaemic, euglycaemic glucose clamp led to an increase in transcapillary escape rate of albumin and a decrease in intravascular mass of albumin. Packed cell volume remained constant, while plasma volume, measured by radiolabeled albumin, decreased. 5. We conclude that the previously reported changes in packed cell volume, plasma volume, intravascular mass of albumin and transcapillary escape rate of albumin during hypoglycaemia may be explained by the combined actions of adrenaline and insulin.
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Moss, I. R., and J. G. Inman. "Neurochemicals and respiratory control during development." Journal of Applied Physiology 67, no. 1 (July 1, 1989): 1–13. http://dx.doi.org/10.1152/jappl.1989.67.1.1.
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During ontogeny, the central nervous system undergoes neuronal growth, regression, and remodeling. The development of neurotransmitter and modulator systems is a plastic process with individual temporal characteristics for each system. These characteristics include the synthesis, degradation, or uptake of neurochemicals and, largely independently, the appearance of their receptors. Message transmission during ontogeny is compounded by the variable development of these systems and by the coexistence and cofunction among these chemicals. Nine neurochemical systems are discussed: adenosine, gamma-aminobutyric acid, opioids, prostaglandins, serotonin, progesterone, substance P, thyrotropin-releasing hormone, and the catecholamines. The possible role of each of these in natural perinatal respiratory control is evaluated according to predetermined criteria. These include the presence of a substance system in respiratory-related regions, physiologically appropriate changes in its concentration in these regions, elicitation of respiratory effects by agonists and antagonists, and abolition with an antagonist of the effect of a substance during its presumed activation by a physiological process. It is suggested that excessive levels of suppressant neuromodulators or an imbalance among neurochemicals can partly explain the special features of respiratory control in the perinatal period.
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Moraska, Albert, Robin A. Pollini, Karen Boulanger, Marissa Z. Brooks, and Lesley Teitlebaum. "Physiological Adjustments to Stress Measures Following Massage Therapy: A Review of the Literature." Evidence-Based Complementary and Alternative Medicine 7, no. 4 (2010): 409–18. http://dx.doi.org/10.1093/ecam/nen029.
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Use of massage therapy by the general public has increased substantially in recent years. In light of the popularity of massage therapy for stress reduction, a comprehensive review of the peer-reviewed literature is important to summarize the effectiveness of this modality on stress-reactive physiological measures. On-line databases were searched for articles relevant to both massage therapy and stress. Articles were included in this review if (i) the massage therapy account consisted of manipulation of soft tissues and was conducted by a trained therapist, and (ii) a dependent measure to evaluate physiological stress was reported. Hormonal and physical parameters are reviewed. A total of 25 studies met all inclusion criteria. A majority of studies employed a 20–30 min massage administered twice-weekly over 5 weeks with evaluations conducted pre-post an individual session (single treatment) or following a series of sessions (multiple treatments). Single treatment reductions in salivary cortisol and heart rate were consistently noted. A sustained reduction for these measures was not supported in the literature, although the single-treatment effect was repeatable within a study. To date, the research data is insufficient to make definitive statements regarding the multiple treatment effect of massage therapy on urinary cortisol or catecholamines, but some evidence for a positive effect on diastolic blood pressure has been documented. While significant improvement has been demonstrated following massage therapy, the general research body on this topic lacks the necessary scientific rigor to provide a definitive understanding of the effect massage therapy has on many physiological variables associated with stress.
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Wang, Wenping, Ximing Wu, Chung S. Yang, and Jinsong Zhang. "An Unrecognized Fundamental Relationship between Neurotransmitters: Glutamate Protects against Catecholamine Oxidation." Antioxidants 10, no. 10 (September 30, 2021): 1564. http://dx.doi.org/10.3390/antiox10101564.
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Neurotransmitter catecholamines (dopamine, epinephrine, and norepinephrine) are liable to undergo oxidation, which copper is deeply involved in. Catecholamine oxidation-derived neurotoxicity is recognized as a pivotal pathological mechanism in neurodegenerative diseases. Glutamate, as an excitatory neurotransmitter, is enriched in the brain at extremely high concentrations. However, the chemical biology relationship of these two classes of neurotransmitters remains largely unknown. In the present study, we assessed the influences of glutamate on the autoxidation of catecholamines, the copper- and copper-containing ceruloplasmin-mediated oxidation of catecholamines, the catecholamine-induced formation of quinoprotein, catecholamine/copper-induced hydroxyl radicals, and DNA damage in vitro. The results demonstrate that glutamate, at a physiologically achievable molar ratio of glutamate/catecholamines, has a pronounced inhibitory effect on catecholamine oxidation, catecholamine oxidation-evoked hydroxyl radicals, quinoprotein, and DNA damage. The protective mechanism of glutamate against catecholamine oxidation could be attributed to its restriction of the redox activity of copper via chelation. This previously unrecognized link between glutamate, catecholamines, and copper suggests that neurodegenerative disorders may occur and develop once the built-in equilibrium is disrupted and brings new insight into developing more effective prevention and treatment strategies for neurodegenerative diseases.
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PERRY, S. F., C. DAXBOECK, and G. P. DOBSON. "The Effect of Perfusion Flow Rate and Adrenergic Stimulation on Oxygen Transfer in the Isolated, Saline-perfused Head of Rainbow Trout (Salmo Gairdneri)." Journal of Experimental Biology 116, no. 1 (May 1, 1985): 251–69. http://dx.doi.org/10.1242/jeb.116.1.251.
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An isolated, saline-perfused trout head preparation, irrigated with hyperoxic water (PWoλ = 250 Torr), was used to assess diffusion/perfusion limitations to gill oxygen transfer. In the absence of catecholamines, increasing the perfusion flow rate caused a reduction of the partial pressure of oxygen in the dorsal aortic perfusate, indicating diffusion limitations to oxygen uptake. Physiological concentrations of epinephrine stimulated oxygen uptake in a dose-dependent fashion. Moreover, epinephrine elicited a greater effect during increased perfusion flow rate as a result of larger initial diffusion limitations, caused by the increased flow. By using a variety of adrenergic agonists and antagonists, it was demonstrated that beta-receptor stimulation enhanced oxygen uptake whereas alpha-receptor stimulation had no effect. These results are discussed with reference to changes in gill epithelial permeability to oxygen and/or surface area changes.
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PLAYLE, RICHARD C., R. STEPHEN MUNGER, and CHRIS M. WOOD. "Effects of Catecholamines on Gas Exchange and Ventilation in Rainbow Trout (Salmo Gairdneri)." Journal of Experimental Biology 152, no. 1 (September 1, 1990): 353–67. http://dx.doi.org/10.1242/jeb.152.1.353.
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A transient inhibitory effect of catecholamines on relative CO2 excretion, mediated by an inhibition of HCO3− dehydration through the red blood cell (RBC), has been proposed to cause the increase in PaCOCO2 routinely observed after strenuous exercise in fish (‘CO2 retention hypothesis’, Wood and Perry, 1985). To evaluate this idea, trout fitted with arterial cannulae, oral membranes and opercular catheters were placed in ventilation chambers. PaCOCO2 RBC intracellular pH (pHi) and other blood acid-base parameters were monitored from the arterial cannulae. The ventilation chamber system allowed continuous, almost instantaneous, measurements of water ΔO2 and ΔCO2 across the gills, and therefore of respiratory exchange ratio (RE), as well as Δammonia, mean expired pH and ventilation volume (Vw). Physiological doses of adrenaline and noradrenaline (3.2nmolkg−1), designed to duplicate typical post-exercise concentrations, together with appropriate saline controls, were injected into resting fish. Adrenaline caused an immediate hypoventilation, while the response to noradrenaline was biphasic: hyperventilation followed by hypoventilation. With both drugs, ΔO2 and ΔCO2 increased, but RE remained constant (adrenaline) or increased (noradrenaline). There was no evidence of a specific inhibition of CO2 excretion, nor was there any increase in PaCOCO2; changes in RBC pHi were small (noradrenaline) or non-existent (adrenaline). These results confirm those of Steffensen et al. (1987) and do not support the CO2 retention hypothesis. However, the RBCs of resting trout may be relatively insensitive to catecholamines at normal arterial blood pH (pHa).
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Petrov, Nikita, Nadezhda Biryulina, Yuliia Sidorova, and Vladimir Mazo. "A food ingredient containing phytoecdysteroids and polyphenols from quinoa grain: technology and physiological and biochemical evaluation in vivo." E3S Web of Conferences 285 (2021): 05014. http://dx.doi.org/10.1051/e3sconf/202128505014.
Full textAbstract:
An effective technological approach to produce adaptogenic microingredients is to concentrate plant biologically active substances via sorption on various matrices. The aim was to develop and evaluate in vivo the phytoecdysteroids and flavonoids concentrate extracted from quinoa grain and sorbed on the coagulated chicken egg protein. The consecutive extraction of phytoecdysteroids and flavonoids was conducted followed by sorption on the protein. The in vivo experiment was performed during 37 days using Wistar male rats. The developed concentrate was added into the diet of experimental animals in the dose 0.59±0.02 g/100 g of diet. As a stress model we used daily 40-min immobilization and exhaustive 3-hour immobilization at the end of the experiment. Urinary catecholamines content was determined, blood corticosterone, malon dialdehyde, glutathione reductase and superoxide dismutase content was determined. Phytoecdysteroids and flavonoids were concentrated 20 and 80 times respectively compared to the initial raw materials. The concentrate consumption neutralized negative effect of immobilization stress on anxiety level of Wistar rats. The significant decrease in urinary excretion of adrenaline and noradrenaline shows the pronounced adaptogenic effect of the concentrate, whereas phytoecdysteroids and flavonoids act as prostressors activating body antioxidant protection system, what is substantiated by significantly increased blood superoxide dismutase level of experimental animals.
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Bzoskie, L., L. Blount, K. Kashiwai, Y. T. Tseng, W. W. Hay, and J. F. Padbury. "Placental norepinephrine clearance: in vivo measurement and physiological role." American Journal of Physiology-Endocrinology and Metabolism 269, no. 1 (July 1, 1995): E145—E149. http://dx.doi.org/10.1152/ajpendo.1995.269.1.e145.
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The intrauterine clearance rate of catecholamines is higher than in newborn animals or in adults. The separate contributions of the fetus and placenta to this clearance are not known. The placenta is a site of expression of the amine plasma membrane transporters that mediate this process. To determine the physiological role of this placental transporter in vivo, we studied fetal sheep at 123 days with common umbilical vein (UV), fetal arterial (AO), and venous catheters. Tritiated norepinephrine ([3H]NE) was infused to determine the kinetics of placental and fetal NE appearance and clearance rates. Umbilical flow was determined by [3H]NE infusion. Placental and total (fetal-placental) NE clearance rates were determined by measurement of [3H]NE from simultaneously drawn UV and AO samples. Total clearance was 99 +/- 8 ml.kg-1.min-1. Placental fractional [3H]NE extraction was 21% and accounted for 48% of total clearance. Fetal plasma NE production rate was 85 +/- 20 ng.kg-1.min-1. We conclude that placental catecholamine clearance is an important metabolic function of the placenta. This mechanism for clearance of the high fetal production rate of catecholamines is vital for fetal homeostasis. We speculate that derangements in placental catecholamine clearance may explain the exaggerated adverse effects on the fetus of drugs like cocaine, which block catecholamine transport.
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Wilson, John X., Khaled J. Saleh, E. Davindra Armogan, and Ewa J. Jaworska. "Catecholamine and blood pressure regulation by gonadotropin-releasing hormone analogs in amphibians." Canadian Journal of Physiology and Pharmacology 65, no. 12 (December 1, 1987): 2379–85. http://dx.doi.org/10.1139/y87-377.
Full textAbstract:
Analogs of gonadotropin-releasing hormone (GnRH) occur in the brain, plasma, and sympathoadrenal system of anuran amphibians. The present experiments studied the effects of GnRH and [Trp7, Leu8]-GnRH on plasma catecholamines and cardiovascular function in conscious adult bullfrogs (Rana catesbeiana) and cane toads (Bufo marinus). Both GnRH analogs elicited dose-dependent (0.1–1 nmol∙kg−1) increases in arterial norepinephrine, epinephrine, and blood pressure levels when injected intravenously into toads. In bullfrogs, [Trp7, Leu8]-GnRH (1 nmol∙kg−1) increased arterial norepinephrine concentration approximately 10-fold without affecting the concentrations of norepinephrine sulfate, norepinephrine glucuronide, epinephrine, epinephrine sulfate, or epinephrine glucuronide. The noradrenergic response of bullfrogs to [Trp7, Leu8]-GnRH was specific to the neurohormone because it could be inhibited by [D-pGlu1, D-Phe2, D-Trp3,6]-GnRH. The sympathomimetic activities of the GnRH analogs did not depend on changes in temperature, which occur seasonally in natural habitats, because similar noradrenergic responses were observed at 4 and 22 °C. GnRH and [Trp7, Leu8]-GnRH (0.01–10 nmol∙kg−1) did not raise arterial blood pressure in bullfrogs despite their pressor actions in toads. This interspecific difference was remarkable because cardiovascular responses to norepinephrine, angiotensin II, and vasotocin in bullfrogs were similar to those in toads. The parallels between catecholamine and blood pressure responses suggest that epinephrine is the principal mediator of the blood pressure response to native GnRH analogs in toads. In bullfrogs, [Trp7, Leu8]-GnRH mobilizes norepinephrine but not epinephrine, and the noradrenergic effect is insufficient to raise blood pressure. These observations are consistent with a physiological role for native GnRH analogs in the regulation of the sympathoadrenal system in anuran amphibians.
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Jern, Christina, Karin Manhem, Elsa Eriksson, Lilian Tengborn, Bo Risberg, and Sverker Jern. "Hemostatic Responses to Mental Stress during the Menstrual Cycle." Thrombosis and Haemostasis 66, no. 05 (1991): 614–18. http://dx.doi.org/10.1055/s-0038-1646469.
Full textAbstract:
SummaryTo study the effect of sex hormones on the hemostatic responses to stress, blood samples were collected before, during, and after 20 min of mental stress from 9 healthy, non-smoking female volunteers, examined in the follicular and luteal phase. Mental stress caused significant increases in heart rate, blood pressure, and plasma catecholamines. In addition, analysis of variance indicated significant changes of leukocyte count, hematocrit, fibrinogen, von Willebrand factor antigen, t-PA activity and antigen in response to the stress test. However, in contrast to a male group previously investigated, there were no significant changes in factor VII coagulant activity in either menstrual phase. Overall the responses were more pronounced in the luteal as compared to the follicular phase. The findings support the concept that both gender and physiological variations in female sex hormones may modulate hemostatic responses to psychosocial stress.
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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.
Full textAbstract:
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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Eckel, J., and H. Reinauer. "Modulation of transmembrane potential of isolated cardiac myocytes by insulin and isoproterenol." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 2 (August 1, 1990): H554—H559. http://dx.doi.org/10.1152/ajpheart.1990.259.2.h554.
Full textAbstract:
Isolated muscle cells from adult rat heart have been used to study the effects of insulin and catecholamines on transmembrane potential by following triphenylmethylphosphonium cation uptake. Insulin was found to hyperpolarize the cells with a maximal effect of 3.2 +/- 0.7 mV (n = 4) at an insulin concentration of 3 x 10(-9) mol/l. This insulin action was fully antagonized by isoproterenol (10(-5) mol/l), which depolarized the cardiocytes in a dose-dependent fashion with a maximal effect of 9.5 +/- 2.2 mV. Treatment of cardiocytes with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid or CsCl resulted in a total loss of insulin action, whereas isoproterenol action was not affected. Cardiac myocytes from streptozotocin diabetic rats exhibited an unaltered hyperpolarization by insulin within the physiological concentration range. Isoproterenol now induced a biphasic response with a significant hyperpolarization at low doses and a decreased depolarization at maximal concentrations. In conclusion, 1) hormonal modulation of cardiac myocyte membrane potentials involves hyperpolarization by insulin and depolarization by beta-agonists, 2) insulin action appears to be related to an increased potassium conductance and may be antagonized by beta-stimulation, and 3) membrane potential modulation may be profoundly altered in the diabetic state.
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Matušková, L., and M. Javorka. "Adrenergic receptors gene polymorphisms and autonomic nervous control of heart and vascular tone." Physiological Research, S4 (January 30, 2022): S495—S510. http://dx.doi.org/10.33549/physiolres.934799.
Full textAbstract:
Adrenergic receptors (ARs) are the primary targets of catecholamines released from the sympathetic nerve endings during their activation. ARs play a central role in autonomic nervous system and serve as important targets of widely used drugs. Several ARs gene polymorphisms were found to be associated with cardiovascular disease in previous clinical studies. Although more precise mechanism of the polymorphisms influence on autonomic control of cardiovascular system was studied in many previous physiological studies, their results are not unequivocal. This paper reviews the results of clinical and physiological studies focused on the impact of selected common single nucleotide polymorphisms of ARs genes involved in sympathetic control on cardiovascular system and its control. In summary, many studies assessed only a very limited range of cardiovascular control related parameters providing only very limited view on the complex cardiovascular control. The overview of partially contradicting results underlines a need to examine wider range of cardiovascular measures including their reactivity under various stress conditions requiring further study. It is expected that an effect of one given polymorphism is not very prominent, but it is suggested that even subtle differences in cardiovascular control could – on a longer time scale – lead to the development of severe pathological consequences.
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Motais, R., F. Garcia-Romeu, and F. Borgese. "The control of Na+/H+ exchange by molecular oxygen in trout erythrocytes. A possible role of hemoglobin as a transducer." Journal of General Physiology 90, no. 2 (August 1, 1987): 197–207. http://dx.doi.org/10.1085/jgp.90.2.197.
Full textAbstract:
It has previously been shown that addition of catecholamines to a suspension of trout erythrocytes induces an enlargement of the cells owing to an uptake of NaCl mediated by a cAMP-dependent, amiloride-sensitive Na+/H+ exchange. In this article, we show that the change in cell volume induced by catecholamines is much greater when the erythrocytes are incubated in N2 than when they are in O2. This difference is explained by an inhibition of the cAMP-dependent Na+/H+ exchange by O2. The inhibition is not reversed in cells incubated in O2 but poisoned with cyanide. It cannot be explained by a difference in the content of cAMP in O2 and in N2. In a CO atmosphere, in which the cells are anoxic, swelling and Na permeability are not increased as they are in N2: in CO, the cells behave as they do in O2. Moreover, cells previously exposed to CO and then put in an N2 atmosphere do not show the expected increase in Na+/H+ exchange. This strongly indicates that the binding of CO to hemoglobin, which persists during the subsequent exposure to N2, is the primary event responsible for the inhibition. As CO substitutes for O2 in binding to hemoglobin, the effect of O2 in the control of Na+/H+ exchange is probably explained by this interaction with heme. (Allen and McManus [1968. Biophysical Journal. 8:125a] previously described a similar effect of CO on passive Na permeability in duck red cells.) It is proposed that the hemoglobin, by interacting differently, according to its degree of oxygenation, with the cytoplasmic segment of band 3 protein, may influence some transport function, such as Na+/H+ exchange. The physiological significance of a control of Na+/H+ exchange by molecular O2 is discussed.
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Currie, Kevin P. M., and Aaron P. Fox. "Voltage-Dependent, Pertussis Toxin Insensitive Inhibition of Calcium Currents by Histamine in Bovine Adrenal Chromaffin Cells." Journal of Neurophysiology 83, no. 3 (March 1, 2000): 1435–42. http://dx.doi.org/10.1152/jn.2000.83.3.1435.
Full textAbstract:
Histamine is a known secretagogue in adrenal chromaffin cells. Activation of G-protein linked H1 receptors stimulates phospholipase C, which generates inositol trisphosphate leading to release of intracellular calcium stores and stimulation of calcium influx through store operated and other channels. This calcium leads to the release of catecholamines. In chromaffin cells, the main physiological trigger for catecholamine release is calcium influx through voltage-gated calcium channels ( I Ca). Therefore, these channels are important targets for the regulation of secretion. In particular N- and P/Q-type I Ca are subject to inhibition by transmitter/hormone receptor activation of heterotrimeric G-proteins. However, the direct effect of histamine on I Ca in chromaffin cells is unknown. This paper reports that histamine inhibited I Cain cultured bovine adrenal chromaffin cells and this response was blocked by the H1 antagonist mepyramine. With high levels of calcium buffering in the patch pipette solution (10 mM EGTA), histamine slowed the activation kinetics and inhibited the amplitude of I Ca. A conditioning prepulse to +100 mV reversed the kinetic slowing and partially relieved the inhibition. These features are characteristic of a membrane delimited, voltage-dependent pathway which is thought to involve direct binding of G-protein βγ subunits to the Ca channels. However, unlike virtually every other example of this type of inhibition, the response to histamine was not blocked by pretreating the cells with pertussis toxin (PTX). The voltage-dependent, PTX insensitive inhibition produced by histamine was modest compared with the PTX sensitive inhibition produced by ATP (28% vs. 53%). When histamine and ATP were applied concomitantly there was no additivity of the inhibition beyond that produced by ATP alone (even though the agonists appear to activate distinct G-proteins) suggesting that the inhibition produced by ATP is maximal. When experiments were carried out under conditions of low levels of calcium buffering in the patch pipette solution (0.1 mM EGTA), histamine inhibited I Ca in some cells using an entirely voltage insensitive pathway. We demonstrate that activation of PTX insensitive G-proteins (most likely Gq) by H1 receptors inhibits I Ca. This may represent a mechanism by which histamine exerts inhibitory (in addition to previously identified stimulatory) effects on catecholamine release.
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Dzeka, T. Nancy, and J. Malcolm O. Arnold. "Prostaglandin modulation of venoconstriction to physiological stress in normals and heart failure patients." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 3 (March 1, 2003): H790—H797. http://dx.doi.org/10.1152/ajpheart.00572.2001.
Full textAbstract:
Prostaglandins released from blood vessels modulate vascular tone, and inhibition of their production during exogenous infusions of catecholamines causes increased venoconstriction. To determine the influence of prostaglandin production on venoconstriction during physiological stimuli known to cause sympathetic activation, and to assess its importance in chronic heart failure (CHF), we studied 11 normal subjects (62 ± 4 yr) and 14 patients with CHF (64 ± 2 yr, left ventricular ejection fraction 23 ± 1%, New York Heart Association classes II and III) (means ± SE). Dorsal hand vein distension was measured during mental arithmetic (MA), cold pressor test (CPT), and lower body negative pressure (LBNP; −10 and −40 mmHg), with saline infusion in one hand and local indomethacin (cyclooxygenase inhibitor) infusion (3 μg/min) in the other. Acetylcholine (0.01–1 nmol/min) dilated veins preconstricted with PGF2α in normals but, consistent with endothelial dysfunction, barely did so in CHF patients ( P = 0.001). Nonendothelial venodilation to sodium nitroprusside (0.3–10 nmol/min) was not different between normals and CHF patients. Resting venous norepinephrine levels were higher in CHF patients (2,812 ± 420 pmol/l) than normals (1,418 ± 145 pmol/l, P = 0.007). In normals, indomethacin caused increased venoconstriction to MA (from 4.9 ± 1.5 to 19.2 ± 4.5%, P = 0.022) and CPT (from 2.9 ± 3.8 to 17.6 ± 4.2%, P = 0.007). In CHF, indomethacin caused increased venoconstriction to MA (from 6.6 ± 3.9% to 19.0 ± 4.5%, P = 0.014), CPT (from 9.6 ± 2.1% to 20.1 ± 3.7%, P = 0.001), and −40 mmHg LBNP (from 10.7 ± 3.0% to 23.2 ± 3.8%, P= 0.041). Control responses for all tests were not different between normals and CHF patients. The effects of indomethacin on venoconstriction to MA and CPT were not different between normals and CHF patients, but venoconstriction to −40 mmHg LBNP was accentuated in CHF patients ( P = 0.036). Inhibition of prostaglandins by indomethacin significantly enhances hand vein constriction to physiological stimuli in both normals and CHF patients, although a differential effect exists for LBNP.
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Taylor, A. H., G. St J. Whitley, and S. S. Nussey. "The interaction of arginine vasopressin and oxytocin with bovine adrenal medulla cells." Journal of Endocrinology 121, no. 1 (April 1989): 133–39. http://dx.doi.org/10.1677/joe.0.1210133.
Full textAbstract:
ABSTRACT Binding of [3H]arginine vasopressin (AVP) and [3H]oxytocin to primary monolayer cultures of bovine adrenal chromaffin cells was time-dependent, and the binding sites for each peptide were specific and saturable. Studies with the V1 AVP antagonist d(CH2)5Tyr(Me)2-AVP, the V2 agonist 1-deamino-8-d-AVP and the V2 antagonist d(CH2)5d-Leu2,Val4-AVP indicated that the AVP receptor was V1 in specificity. Scatchard plots showed that each ligand interacted with a single high-affinity, low-capacity binding site: oxytocin dissociation constant (Kd) 0·29 ± 0·02 nmol/l, maximum binding capacity (Bmax) 7·6 ± 0·2 fmol/106 cells (or 4500 ± 102 sites/cell) (n = 3); AVP Kd 0·09±0·02 nmol/l, Bmax 5·1±0·63 fmol/106 cells (or 3050 ± 318 sites/cell) (n = 3). Although forskolin in concentrations from 1 nmol/l to 1 mmol/l stimulated cyclic AMP (cAMP) production in isolated chromaffin cells, this did not result in detectable catecholamine release. Neither AVP nor oxytocin in concentrations between 10 pmol/l and 10 μmol/l stimulated cAMP production in these cells. Vasopressin in concentrations as low as 10 pmol/l stimulated a sixfold increase in total inositol phosphates; the dose–response curve was triphasic. Oxytocin had little effect on total inositol phosphate accumulation at low concentrations, but concentrations above micromolar stimulated total inositol phosphate production approximately fourfold. There was no measurable release of catecholamines in response to either peptide. The physiological consequences of these AVP-induced changes in inositol phosphate concentrations remain to be elucidated. Journal of Endocrinology (1989) 121, 133–139
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Xu, Ming, Qiulin Zhang, Qi Wang, Di Pan, Mingxing Ding, and Yi Ding. "The Characteristics and Distribution of α2D-, α2B- and α2C-Adrenoceptor Subtypes in Goats." Animals 12, no. 5 (March 7, 2022): 664. http://dx.doi.org/10.3390/ani12050664.
Full textAbstract:
α2-Adrenegic receptors (α2Rs) are important presynaptic modulators of central noradrenergic function (auto receptors) and postsynaptic mediators of many of the widespread effects of catecholamines and related drugs. Studies have shown that ruminants (such as goats and cattle) express special α2DR subtypes in addition to α2BR and α2CR. Real-time quantitative PCR and Western blotting were used to investigate the distribution and density of α2R in different nuclei of the goat central nervous system, selected regions of the spinal cord (L4-L6), and in various peripheral tissues. α2-AR subtype-specific antibodies were injected intrathecally and intracerebroventricularly into the tested goats to block the corresponding subtype of receptors. Pain threshold and physiological parameters were evaluated to explore the functional characteristics of α2BR, α2CR and α2DR in goats. Our results suggest that the expression of the mRNAs and proteins of all three α2R subtypes are widely but unevenly distributed in the goat CNS and peripheral tissues. Furthermore, α2DR plays a more important role in α2R-mediated analgesia in goats than α2BR and α2CR, whereas α2CR activation exerts a greater effect on body temperature than α2BR and α2DR.
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Seabrook, Timothy J., Bill Ristevski, Shawn G. Rhind, Pang N. Shek, Jiri Zamecnik, Roy J. Shephard, and John B. Hay. "Epinephrine causes a reduction in lymph node cell output in sheep." Canadian Journal of Physiology and Pharmacology 79, no. 3 (March 1, 2001): 246–52. http://dx.doi.org/10.1139/y00-124.
Full textAbstract:
The lymphatic system has a critical role in the return of fluids, proteins, and cells to the circulatory system. However, the effects of stress, including exercise, on this system have not been adequately studied. We investigated the effect of a physiological dose (1 mg) of epinephrine (Epi) on lymph flow, cell concentration, and lymphocyte subsets in efferent subcutaneous lymph in sheep. Blood leukocyte numbers, differential, lymphocyte subsets, and blood and lymph pools of lymphocytes were determined simultaneously. A significant acute increase in lymph flow was followed by a post-injection decrease in flow and cellular output. No changes in lymphocyte subsets or pools of lymphocytes were seen in either blood or lymph. The timing of elevated plasma and lymph concentrations of Epi and norepinephrine (NE) corresponded with the increased lymph flow. In conclusion, Epi injection caused no change in lymphocyte subset distribution, leukocyte concentration, or pools of lymphocytes. A decrease in lymph flow and cellularity was documented post-injection, indicating that lymphatic tissue has no role in the leukocytosis seen after Epi injection. Lymphocyte retention by lymph nodes, however, may contribute to post-injection lymphopenia.Key words: lymphocyte recirculation, catecholamines, exercise, stress, lymph.
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Thom, S., J. Calvete, R. Hayes, G. Martin, and P. Sever. "Human vascular smooth muscle responses mediated by α2 mechanisms in vivo and in vitro." Clinical Science 68, s10 (January 1, 1985): 147s—150s. http://dx.doi.org/10.1042/cs068s147.
Full textAbstract:
1. The effects of compounds with α2-agonist and α2-antagonist properties on human forearm blood flow and on isolated human arterial segments have been studied. 2. The findings from these studies in vivo and in vitro did not provide evidence in support of the hypothesis that postsynaptic α2-receptors mediate smooth muscle contraction in the tissues under investigation. 3. The constriction of the forearm vascular bed in response to low intra-arterial doses of idazoxan (RX 781094), an α2-antagonist, provides evidence for a physiological role for a presynaptic α2 autoregulatory mechanism. 4. The variability of the forearm vascular responses to higher doses of idazoxan highlights the pitfalls that may have misled previous authors in their interpretation of the results of similar studies. A U-shaped dose-response curve to compounds with mixed α2-and α1-antagonist properties may be constructed, which emphasizes the importance of the dose-dependent selectivity of these antagonists at α2- and α1-receptors. 5. The effect of idazoxan on the responses of arterial segments in vitro to exogenous catecholamines was dependent on the integrity of the endothelium, and provides evidence that α2-receptors may mediate release of the endothelium-derived relaxing factor.