Journal articles on the topic 'Capsaicin Physiological effect'
To see the other types of publications on this topic, follow the link: Capsaicin Physiological effect.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Capsaicin Physiological effect.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Li, Xi Hong, Gui Ming Lei, and Xia Liu. "Effect of Capsaicin-Coated PE Film on Microbiological and Physiological Properties of Rice during Storage." Advanced Materials Research 156-157 (October 2010): 1109–12. http://dx.doi.org/10.4028/www.scientific.net/amr.156-157.1109.
Full textAbstract:
Three repellent coated PE film were development for avoiding storage insects and microorganisms. In this work, the microbiological and physiological properties of tetramethrin, cymperator and capsaicin-coated PE packing for rice grain were investigated. The results showed that the capsaicin-coated PE film was the optimal packaging material to preserve rice grain fresh. After three months storage of rice grain, capsaicin-coated PE inhibited the growth of bacteria and fungi than blank-coated PE, and had the similarly inhibiting roles than potent synthetic insecticide-coated PE packing. Especially, free fatty acid content increasing was decreased in storage of capsaicin-coated PE film, the flavor changes in slow.
2
Sharma, Neha, Huong T. T. Phan, Tsuyoshi Yoda, Naofumi Shimokawa, Mun’delanji C. Vestergaard, and Masahiro Takagi. "Effects of Capsaicin on Biomimetic Membranes." Biomimetics 4, no. 1 (February 13, 2019): 17. http://dx.doi.org/10.3390/biomimetics4010017.
Full textAbstract:
Capsaicin is a natural compound that produces a warm sensation and is known for its remarkable medicinal properties. Understanding the interaction between capsaicin with lipid membranes is essential to clarify the molecular mechanisms behind its pharmacological and biological effects. In this study, we investigated the effect of capsaicin on thermoresponsiveness, fluidity, and phase separation of liposomal membranes. Liposomal membranes are a bioinspired technology that can be exploited to understand biological mechanisms. We have shown that by increasing thermo-induced membrane excess area, capsaicin promoted membrane fluctuation. The effect of capsaicin on membrane fluidity was dependent on lipid composition. Capsaicin increased fluidity of (1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) membranes, while it rigidified DOPC and cholesterol-based liposomes. In addition, capsaicin tended to decrease phase separation of heterogeneous liposomes, inducing homogeneity. We imagine this lipid re-organization to be associated with the physiological warming sensation upon consumption of capsaicin. Since capsaicin has been reported to have biological properties such as antimicrobial and as antiplatelet, the results will help unravel these biological properties.
3
Birsen, İlknur, V. Nimet İzgüt-Uysal, Hakan Soylu, and İsmail Üstünel. "The effect of apelin-13 on gastric ischemia/reperfusion injury: the roles of sensory nerves and vagus nerve." Canadian Journal of Physiology and Pharmacology 98, no. 5 (May 2020): 282–95. http://dx.doi.org/10.1139/cjpp-2019-0502.
Full textAbstract:
Apelin is a peptide that plays a role in physiological processes such as angiogenesis, apoptosis, and proliferation. The aim of this study was to investigate the role of capsaicin-sensitive afferent neurons and vagus in the effect of apelin against ischemia/reperfusion (I/R) injury. The experimental groups were (1) control, (2) I/R, (3) apelin + I/R, (4) vagotomy + I/R, (5) vagotomy + apelin + I/R, (6) capsaicin + I/R, (7) capsaicin + apelin + I/R, (8) lorglumide + I/R, and (9) lorglumide + apelin + I/R. To test the potential gastroprotective effect of apelin-13, apelin-13 (2 mg/kg i.v.) was administered just before both ischemia and reperfusion. A vagotomy was performed 1 week before I/R in the vagotomized groups; capsaicin (125 mg/kg s.c.) was administrated 2 weeks before I/R in the capsaicin-treated groups and lorglumide (5 mg/kg i.p.) was administered 30 min before I/R in the lorglumide-treated groups. After I/R, a variety parameters in gastric tissue were analyzed. cfos expression was determined in brainstem samples. In the I/R group, the lesion index, myeloperoxidase activity, lipid peroxidation, nitric oxide, and tumor necrosis factor-α increased, and mucosal blood flow, prostaglandin-E2, and calcitonin gene related peptide decreased. Apelin prevented the damaging effects of I/R and increased cfos expression in brainstem areas. Vagotomy, capsaicin, and lorglumide largely eliminated the gastroprotective effects of apelin-13. This study showed that sensory nerves and the vagus play regulatory roles in apelin-induced gastroprotection. Cholecystokinin may play a role in the effect of apelin through sensory neurons.
4
Liu, L., W. Zhu, Z. S. Zhang, T. Yang, A. Grant, G. Oxford, and S. A. Simon. "Nicotine Inhibits Voltage-Dependent Sodium Channels and Sensitizes Vanilloid Receptors." Journal of Neurophysiology 91, no. 4 (April 2004): 1482–91. http://dx.doi.org/10.1152/jn.00922.2003.
Full textAbstract:
Nicotine is an alkaloid that is used by large numbers of people. When taken into the body, it produces a myriad of physiological actions that occur primarily through the activation of neuronal nicotinic acetylcholine receptors (nAChRs). We have explored its ability to modulate TRPV1 receptors and voltage-gated sodium channels. The reason for investigating nicotine's effect on sodium channels is to obtain a better understanding of its anti-nociceptive properties. The reasons for investigating its effects on capsaicin-activated TRPV1 channels are to understand how it may modulate this channel that is involved in pain, inflammation, and gustatory physiology. Whole cell patch-clamp recordings from rat trigeminal ganglion (TG) nociceptors revealed that nicotine exhibited anesthetic properties by decreasing the number of evoked action potentials and by inhibiting tetrodotoxin-resistant sodium currents. This anesthetic property can be produced without the necessity of activating nAChRs. Nicotine also modulates TRPV1 receptors inducing a several-fold increase in capsaicin-activated currents in both TG neurons and in cells with heterologously expressed TRPV1 receptors. This sensitizing effect does not require the activation of nAChRs. Nicotine did not alter the threshold temperature (∼41°C) of heat-activated currents in TG neurons that were attributed to arise from the activation of TRPV1 receptors. In this regard, its effect on TRPV1 receptors differs from those of ethanol that has been shown to increase the capsaicin-activated current but decrease the threshold temperature. These studies document several new effects of nicotine on channels involved in nociception and indicate how they may impact physiological processes involving pain and gustation.
5
Patwardhan, Chaitanya A., Eyad Alfa, Su Lu, and Ahmed Chadli. "Progesterone Receptor Chaperone Complex–Based High-Throughput Screening Assay." Journal of Biomolecular Screening 20, no. 2 (September 2, 2014): 223–29. http://dx.doi.org/10.1177/1087057114549147.
Full textAbstract:
Hsp90 and its co-chaperones are known to be important for cancer cell survival. The N-terminal inhibitors of Hsp90 that are in ongoing clinical trials as antitumor agents have unfortunately shown disappointing efficacies in the clinic. Thus, novel inhibitors of the Hsp90 machine with a different mechanism of action are urgently needed. We report here the development of a novel high-throughput screening assay platform to identify small-molecule inhibitors of Hsp90 and its co-chaperones. This assay quantitatively measures the ability of Hsp90 and its co-chaperones to refold/protect the progesterone receptor, a physiological client of Hsp90, in a 96-well plate format. We screened the National Institutes of Health clinical collection drug library and identified capsaicin as a hit molecule. Capsaicin is a Food and Drug Administration–approved drug for topical use in pain management. Cell survival assays showed that capsaicin selectively kills cancer cells and destabilizes several Hsp90 client proteins. Thus, our data may explain the seemingly pleotropic effect of capsaicin.
6
Li, De-Pei, Shao-Rui Chen, and Hui-Lin Pan. "VR1 Receptor Activation Induces Glutamate Release and Postsynaptic Firing in the Paraventricular Nucleus." Journal of Neurophysiology 92, no. 3 (September 2004): 1807–16. http://dx.doi.org/10.1152/jn.00171.2004.
Full textAbstract:
Neurons in the paraventricular nucleus (PVN) are important in regulating autonomic function through projections to the brain stem and spinal cord. Although the vanilloid receptors (VR1) are present in the PVN, their physiological function is scarcely known. In this study, we determined the role of VR1 receptors in the regulation of synaptic inputs and the excitability of spinally projecting PVN neurons. Whole cell patch-clamp recordings were performed on the PVN neurons labeled by a retrograde fluorescence tracer injected into the thoracic spinal cord of rats. Capsaicin significantly increased the frequency of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) without changing the amplitude and decay time constant of mEPSCs. On the other hand, capsaicin had no effect on GABAergic miniature inhibitory postsynaptic currents (mIPSCs). The effect of capsaicin on mEPSCs was abolished by a specific VR1 antagonist, iodo-resiniferatoxin (iodo-RTX), or ruthenium red. Importantly, iodo-RTX per se significantly reduced the amplitude of evoked EPSCs and the frequency of mEPSCs. Removal of extracellular Ca2+, but not Cd2+ treatment, also eliminated the effect of capsaicin on mEPSCs. Furthermore, capsaicin caused a large increase in the firing rate of PVN neurons, and such an effect was abolished in the presence of ionotropic glutamate receptor antagonists. Additionally, the double-immunofluorescence labeling revealed that all of the VR1 immunoreactivity was colocalized with a presynaptic marker, synaptophysin, in the PVN. Thus this study provides the first evidence that activation of VR1 receptors excites preautonomic PVN neurons through selective potentiation of glutamatergic synaptic inputs. Presynaptic VR1 receptors and endogenous capsaicin-like substances in the PVN may represent a previously unidentified mechanism in hypothalamic regulation of the autonomic nervous system.
7
Sugiura, Takeshi, Makoto Tominaga, Hirotada Katsuya, and Kazue Mizumura. "Bradykinin Lowers the Threshold Temperature for Heat Activation of Vanilloid Receptor 1." Journal of Neurophysiology 88, no. 1 (July 1, 2002): 544–48. http://dx.doi.org/10.1152/jn.2002.88.1.544.
Full textAbstract:
Bradykinin (BK) is an inflammatory mediator that plays a pivotal role in pain and hyperalgesia to heat in inflamed tissues by exciting nociceptors and sensitizing them to heat through activation of protein kinase C (PKC). It has been suggested that the capsaicin receptor (VR1), a nociceptor-specific cation channel sensitive to noxious heat, protons, and capsaicin, is a channel that is modified by BK in these effects. In this study, we examined how BK modulates the activity of VR1. We measured VR1 currents using the patch-clamp technique in human embryonic kidney-derived (HEK293) cells expressing VR1 and B2 BK receptor. We found that BK lowered the threshold temperature for activation of VR1 currents in HEK cells down to well below the physiological body temperature in a concentration-dependent manner through PKC activation. We also demonstrated that in capsaicin-sensitive dorsal root ganglion (DRG) neurons the activation threshold of heat-induced current, which is considered to be VR-1 mediated, was lowered by BK and that this effect was also mediated by PKC. These data further support the supposition that modulation of VR1 is a mechanism for the BK-induced excitation of nociceptors and their sensitization to heat.
8
Kanazawa, H., H. Kamoi, T. Kawaguchi, S. Shoji, T. Fujii, S. Kudoh, K. Hirata, and J. Yoshikawa. "PAMP is a novel inhibitor of the tachykinin release in the airway of guinea pigs." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 6 (June 1, 1997): L1066—L1069. http://dx.doi.org/10.1152/ajplung.1997.272.6.l1066.
Full textAbstract:
Proadrenomedullin NH2-terminal 20 peptide (PAMP), a newly identified hypotensive peptide, may play physiological roles in airway and cardiovascular controls. This study was designed to determine the mechanism responsible for the bronchoprotective effects of PAMP on capsaicin-induced bron-choconstriction in anesthetized guinea pigs. PAMP (10(-8)-10(-6) M) significantly inhibited capsaicin-induced bronchoconstriction in a dose-dependent manner. The bronchoprotective effect of PAMP (10(-6) M) was as large as that of isoproterenol (10(-7) M) and lasted > 10 min. The concentration of immunoreactive substance P (SP) in bronchoalveolar lavage fluid after administration of capsaicin (4 x 10(-6) M) was 120 +/- 10 fmol/ml. PAMP significantly inhibited the release of immunoreactive SP in a dose-dependent manner (60 +/- 6 fmol/ml for (10(-6) M PAMP, P < 0.01; 84 +/- 6 fmol/ml for 10(-7) M PAMP, P < 0.01; and 95 +/- 6 fmol/ml for 10(-8) M PAMP, P < 0.05). PAMP (10(-6) M) did not significantly affect exogenous neurokinin A (NKA) or NKA + SP-induced bronchoconstriction, whereas isoproterenol (10(-7) M) significantly inhibited exogenous tachykinin-induced bronchoconstriction. These findings suggest that the bronchoprotective effects of PAMP are mainly due to inhibition of the release of tachykinins at airway C-fiber endings.
9
Raybould, H. E., and Y. Tache. "Cholecystokinin inhibits gastric motility and emptying via a capsaicin-sensitive vagal pathway in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 255, no. 2 (August 1, 1988): G242—G246. http://dx.doi.org/10.1152/ajpgi.1988.255.2.g242.
Full textAbstract:
The pathway by which cholecystokinin octapeptide (CCK-8) inhibits motility of the proximal stomach and the role of this pathway in the CCK-induced delay in gastric emptying of a liquid meal has been studied in rats by selective destruction of vagal afferent C-fibers using bilateral perineural application of the sensory neurotoxin, capsaicin, 3 or 4 days prior to the experiment. The capsaicin treatment significantly attenuated the decrease in intragastric pressure in urethan-anesthetized rats in response to CCK-8 (0.1-100 pmol iv) compared with vehicle-treated controls. Removal of the celiac-superior mesenteric ganglion completely abolished the inhibitory action of CCK-8 on gastric motility in these rats. In contrast, only celiac ganglionectomy in combination with vagotomy abolished the CCK-8 effect in vehicle-treated controls. Intravenous injection of CCK-8 (300 pmol) 5 min before intragastric administration of a methylcellulose solution decreased gastric emptying by 55% in conscious control or vehicle-treated rats. Perivagal capsaicin treatment abolished the delay in gastric emptying induced by CCK-8. In addition, capsaicin treatment alone significantly increased gastric emptying. These results demonstrate that CCK-8 decreases gastric motility in the gastric corpus and delays gastric emptying by a capsaicin-sensitive vagal afferent pathway. These same afferent fibers may also play a physiological role in the gastric emptying of liquids.
10
Lin, Qing, Jiri Palec̆ek, Veronika Palec̆ková, Yuan Bo Peng, Jing Wu, Minglei Cui, and William D. Willis. "Nitric Oxide Mediates the Central Sensitization of Primate Spinothalamic Tract Neurons." Journal of Neurophysiology 81, no. 3 (March 1, 1999): 1075–85. http://dx.doi.org/10.1152/jn.1999.81.3.1075.
Full textAbstract:
Nitric oxide mediates the central sensitization of primate spinothalamic tract neurons. Nitric oxide (NO) has been proposed to contribute to the development of hyperalgesia by activating the NO/guanosine 3′,5′-cyclic monophosphate (cGMP) signal transduction pathway in the spinal cord. We have examined the effects of NO on the responses of primate spinothalamic tract (STT) neurons to peripheral cutaneous stimuli and on the sensitization of STT cells following intradermal injection of capsaicin. The NO level within the spinal dorsal horn was increased by microdialysis of a NO donor, 3-morpholinosydnonimine (SIN-1). SIN-1 enhanced the responses of STT cells to both weak and strong mechanical stimulation of the skin. This effect was preferentially on deep wide dynamic range STT neurons. The responses of none of the neurons tested to noxious heat stimuli were significantly changed when SIN-1 was administered. Intradermal injection of capsaicin increased dramatically the content of NO metabolites, [Formula: see text] within the dorsal horn. This effect was attenuated by pretreatment of the spinal cord with a nitric oxide synthase (NOS) inhibitor, NG-nitro-l-arginine methyl ester (l-NAME). Sensitization of STT cells induced by intradermal injection of capsaicin was also prevented by pretreatment of the dorsal horn with the NOS inhibitors, l-NAME or 7-nitroindazole. Blockade of NOS did not significantly affect the responses of STT cells to peripheral stimulation in the absence of capsaicin injection. The data suggest that NO contributes to the development and maintenance of central sensitization of STT cells and the resultant mechanical hyperalgesia and allodynia after peripheral tissue damage or inflammation. NO seems to play little role in signaling peripheral stimuli under physiological conditions.
11
Jimba, M., W. A. Skornik, C. R. Killingsworth, N. C. Long, J. D. Brain, and S. A. Shore. "Role of C fibers in physiological responses to ozone in rats." Journal of Applied Physiology 78, no. 5 (May 1, 1995): 1757–63. http://dx.doi.org/10.1152/jappl.1995.78.5.1757.
Full textAbstract:
The purpose of this study was to evaluate the role of C fibers in airway responsiveness after exposure to ozone (O3) in rats. The role of C fibers in the decreases in heart rate (HR) and core body temperature (Tc) that occur after inhalation of O3 was also examined. Neonatal rats were treated with capsaicin (Cap) or the vehicle used to dissolve capsaicin (Veh). Cap has been shown to cause permanent destruction of C fibers. When they reached adulthood, conscious minimally restrained rats were exposed to 2 ppm O3 or to air for 3 h. Two hours after the cessation of exposure, rats were anesthetized and instrumented for the measurement of pulmonary mechanics and airway responsiveness to inhaled aerosolized methacholine. O3 had no effect on baseline pulmonary conductance (GL) in either Veh or Cap rats but did cause a decrease in dynamic compliance (Cdyn) in Cap rats (P < 0.05). In Cap rats, O3 exposure caused a marked increase in airway responsiveness; the doses of inhaled aerosolized methacholine required to decrease GL and Cdyn by 50% were 6.5-fold and 9.8-fold lower in O3-compared with air-exposed rats (P < 0.005). In contrast, in Veh rats, O3 did not alter responsiveness. During O3 exposure, there was a profound, almost 50%, decrease in HR as measured with implanted electrodes. A decrease in Tc (measured with a rectal probe) of approximately 2.5 degrees C also occurred during O3 exposure. There was no significant effect of Cap pretreatment on the magnitude of these O3-induced changes in HR and Tc. Our results are consistent with the hypothesis that C fibers act to inhibit the development of hyperresponsiveness elicited by O3 inhalation but do not contribute to O3-induced changes in HR or Tc.
12
Padilha, Camila S., Francois Billaut, Caique Figueiredo, Valéria Leme Gonçalves Panissa, Fabrício Eduardo Rossi, and Fabio S. Lira. "Capsaicin Supplementation during High-intensity Continuous Exercise: A Double-blind Study." International Journal of Sports Medicine 41, no. 14 (July 21, 2020): 1061–66. http://dx.doi.org/10.1055/a-1088-5388.
Full textAbstract:
AbstractTo investigate the effect of acute capsaicin (CAP) supplementation on time to exhaustion, physiological responses and energy systems contribution during continuous high-intensity exercise session in runners. Fifteen recreationally-trained runners completed two randomized, double-blind continuous high-intensity exercises at the speed eliciting 90% V̇O2peak (90% s V̇O2peak), 45 minutes after consuming capsaicin or an isocaloric placebo. Time to exhaustion, blood lactate concentration, oxygen consumption during and 20-min post-exercise, energy systems contribution, time to reach V̇O2peak, heart rate and the rate of perceived exertion (RPE) were evaluated. There was no significant difference between conditions for time to reach V̇O2peak (CAP:391.71±221.8 vs. PLA:298.20±174.5 sec, ES:0.58, p=0.872), peak lactate (CAP:7.98±2.11 vs. PLA:8.58±2.15 µmol, ES:−0.28, p=0.257), time to exhaustion (CAP:654.28±195.44 vs. PLA:709.20±208.44 sec, ES:−0.28, p=0.462, end-of-exercise heart rate (CAP:177.6±14.9 vs. PLA:177.5±17.9 bpm, ES:−0.10, p=0.979) and end-of-exercise RPE (CAP: 19±0.8 vs. PLA: 18±2.4, ES: 0.89, p=0.623). In conclusion, acute CAP supplementation did not increase time to exhaustion during high-intensity continuous exercise nor alter physiological responses in runners.
13
Lu, Y., and C. Owyang. "Secretin at physiological doses inhibits gastric motility via a vagal afferent pathway." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 6 (June 1, 1995): G1012—G1016. http://dx.doi.org/10.1152/ajpgi.1995.268.6.g1012.
Full textAbstract:
Secretin is an important modulator of gastric motility. In this study, we investigated the site(s) and mechanism(s) of action of secretin to inhibit gastric motility, using an in vivo rat model. Intragastric pressure response to graded doses of secretin was recorded in anesthetized rats by a balloon attached to a catheter passed through an incision in the duodenum into the body of the stomach. The intragastric pressure was set at 10 cmH2O with balloon distension. Intravenous infusion of secretin (1.4, 2.8, 5.6, 11.2, and 22.4 pmol.kg-1.h-1) decreased intragastric pressure in a dose-dependent manner. The threshold dose was 2.8 pmol.kg-1.h-1, and the effective dose at 50% (ED50) was 5.6 pmol.kg-1.h-1, which produced physiological levels of plasma secretin. Pretreatment with hexamethonium (10 mg/kg) markedly reduced gastric motor response to secretin (5.6 pmol.kg-1.h-1). Bilateral truncal vagotomy also significantly diminished gastric motor responses to secretin. In contrast, secretin (5.6 pmol.kg-1.h-1) had no effect on gastric contraction evoked by electrical vagal stimulation (1.25-5 Hz) or carbachol (10(-6) to 3 x 10(-5) M). These observations indicate that physiological concentrations of secretin act via stimulation of presynaptic cholinergic neurons in a vagally mediated pathway. In subsequent studies, we demonstrated that perivagal treatment 4 days before with the sensory neurotoxin, capsaicin, abolished gastric motor response to secretin but did not affect contraction evoked by electrical vagal stimulation. Similarly, we also showed that gastroduodenal application of capsaicin for 30 min also markedly reduced gastric response to secretin. These observations indicate that physiological doses of secretin act on vagal afferent pathways originating from the gastroduodenal mucosa to induce gastric relaxation.
14
Kwon, Hyeok Y., Ta-Min Chang, Kae Y. Lee, and William Y. Chey. "Vagus nerve modulates secretin binding sites in the rat forestomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 4 (April 1, 1999): G1052—G1058. http://dx.doi.org/10.1152/ajpgi.1999.276.4.g1052.
Full textAbstract:
Secretin is well known for its inhibitory action on gastric motility. It has been reported that secretin in a physiological dose inhibits gastric motility through mediation by the vagal afferent pathway. Secretin also elicited relaxation of carbachol-stimulated rat forestomach muscle strips by binding to its receptors, suggesting a direct action on this peripheral tissue. We hypothesized that vagal input may affect the action of secretin by modulating the level of secretin receptor in the forestomach. Several treatments, including vagal ligation, vagotomy, perivagal application of capsaicin or colchicine, intravenous infusion of tetrodotoxin, and intraperitoneal injection of atropine, were performed to investigate their effects on secretin receptor binding to forestomach membranes. Specific binding of125I-labeled secretin to forestomach membranes was significantly decreased (45%) by vagal ligation, vagotomy (50%), or perivagal colchicine treatment (40%). On the contrary, specific binding of125I-secretin was not affected by perivagal capsaicin treatment, intravenous infusion of tetrodotoxin, or intraperitoneal injection of atropine. By Scatchard analysis of the binding data, the capacity of the high-affinity binding sites in forestomach membranes was found to decrease significantly after vagal ligation compared with membranes from the sham-operated group. However, the affinity at the high-affinity binding sites, the binding parameters of the low-affinity binding sites, and binding specificity were not changed. Vagal ligation but not perivagal capsaicin treatment reduced the inhibitory effect of secretin on bethanechol-stimulated contraction of isolated forestomach muscle strips, causing a right shift in the dose-response curve. These results suggest that vagal input through axonal transport plays a significant role on secretin action by modulating the capacity of secretin binding sites (but not affinity or specificity), at least in rat forestomach.
15
Maruyama, Ikuro, Kentaro Soejima, Toshiaki Shimi, Kazuhiro Abeyama, and Teruto Hashiguchi. "Functional Vanilloid Receptor VR1 Is Expressed on Megakaryocytes and Platelets, and Acts as a Sensor for Hypertheimia Generating Endocannabinoids." Blood 104, no. 11 (November 16, 2004): 4001. http://dx.doi.org/10.1182/blood.v104.11.4001.4001.
Full textAbstract:
Abstract Recent investigations have been revealing that platelet can sense shear stress and cold stimulation. These mechanical and physical stimuli alter the platelet functions, including induction of activation and irreversible dysfunction. These data may suggest that platelets, most small-sized cells, can efficiently circulate in the microcirculatory vasculature, and can sense the peripheral physical conditions including temperature. Here we show that human megakaryocytic cell line, MEG-01 and platelets express vanilloid receptor VR1, a receptor for capsaicin. It has been identified that VR1 is linked to thermal sensor, and this can sense hyperthermia around 43 °. Therefore we examined the physiological significance of VR1 expressed on MEG-01 and platelets. First we identified the expression of VR1 on human platelets and MEG-01 by immunoblotting, flowcytometer and RT-PCR, and identified the expression of VR1 on these cells. Hyperthermia stimulation of MEG-01 at 40–43 ° generated a endocannabinoids, 2-arachidonylglycerol(2-AG) and anandamide. Since this effect of hyperthermia stimulation was abolished by the incubation with capsazepine, an antagonistic analogue of capsaicin, it was suggested that the effect of hyperthermia might through VR1. It is well known that 2-AG and anandamide act on their specific receptors, CB1, CB2 and VR1 expressed on various cell-types, and act as an endocannabinoids, and accomplish diverse physiological functions, including vessel dilatation. Hyperthermia stimulation also affected the cell-cycle and induced G1-phase arrest in MEG-01 cells, partially through autocrine manner of generated endocannabinoids by acting of CB1 and CB2 receptors. Moreover prolonged hyperthermia stimulation up to 6 hours induced cellular apoptosis in MEG-01 by releasing cytocrome C and resulting caspase cascade activation. Based on these results, we hypothesize that VR1 on platelets may act as a hyperthermal sensor and generate endocannabinoid, and this may regulate the diverse systems including vessel functions.
16
Simonsen, Henrik Toft. "Article Commentary: Capsaicin—the Hot and Spicy Diet Turned Mild and Effective by Glycosylation." Biochemistry Insights 2 (January 2009): BCI.S3064. http://dx.doi.org/10.4137/bci.s3064.
Full textAbstract:
Shimoda and coworkers 1 published a paper on the pharmacological properties of glycosides of the peppery compound capsaicin (1) and its derivative 8-nordihydrocapsaicin (2). In their paper they conclude that the β-glucoside and β-maltoside of 1 and the β-glucoside of 2 still have the same potent anti-obese activity but further studies are needed to determine the physiological effect. Shimoda et al. 1 use glycosylation to make a drug candidate more water soluble to promote their research for new drug candidates within the chemical group of capsaicinoids. Their findings support that this is a plausible way to enhance both bioavailability and “drug-likeliness” properties of drug candidates. This is indeed an interesting approach which should be pursued further and by many more.
17
Akiba, Yasutada, Chikako Watanabe, Misa Mizumori, and Jonathan D. Kaunitz. "Luminal l-glutamate enhances duodenal mucosal defense mechanisms via multiple glutamate receptors in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 4 (October 2009): G781—G791. http://dx.doi.org/10.1152/ajpgi.90605.2008.
Full textAbstract:
Presence of taste receptor families in the gastrointestinal mucosa suggests a physiological basis for local and early detection of a meal. We hypothesized that luminal l-glutamate, which is the primary nutrient conferring fundamental umami or proteinaceous taste, influences mucosal defense mechanisms in rat duodenum. We perfused the duodenal mucosa of anesthetized rats with l-glutamate (0.1–10 mM). Intracellular pH (pHi) of the epithelial cells, blood flow, and mucus gel thickness (MGT) were simultaneously and continuously measured in vivo. Some rats were pretreated with indomethacin or capsaicin. Duodenal bicarbonate secretion (DBS) was measured with flow-through pH and CO2 electrodes. We tested the effects of agonists or antagonists for metabotropic glutamate receptor (mGluR) 1 or 4 or calcium-sensing receptor (CaSR) on defense factors. Luminal l-glutamate dose dependently increased pHi and MGT but had no effect on blood flow in the duodenum. l-glutamate (10 mM)-induced cellular alkalinization and mucus secretion were inhibited by pretreatment with indomethacin or capsaicin. l-glutamate effects on pHi and MGT were mimicked by mGluR4 agonists and inhibited by an mGluR4 antagonist. CaSR agonists acidified cells with increased MGT and DBS, unlike l-glutamate. Perfusion of l-glutamate with inosinate (inosine 5′-monophosphate, 0.1 mM) enhanced DBS only in combination, suggesting synergistic activation of the l-glutamate receptor, typical of taste receptor type 1. l-leucine or l-aspartate had similar effects on DBS without any effect on pHi and MGT. Preperfusion of l-glutamate prevented acid-induced cellular injury, suggesting that l-glutamate protects the mucosa by enhancing mucosal defenses. Luminal l-glutamate may activate multiple receptors and afferent nerves and locally enhance mucosal defenses to prevent subsequent injury attributable to acid exposure in the duodenum.
18
Kirschstein, Timo, Wolfgang Greffrath, Dietrich Büsselberg, and Rolf-Detlef Treede. "Inhibition of Rapid Heat Responses in Nociceptive Primary Sensory Neurons of Rats by Vanilloid Receptor Antagonists." Journal of Neurophysiology 82, no. 6 (December 1, 1999): 2853–60. http://dx.doi.org/10.1152/jn.1999.82.6.2853.
Full textAbstract:
Recent studies demonstrated that heat-sensitive nociceptive primary sensory neurons respond to the vanilloid receptor (VR) agonist capsaicin, and the first cloned VR is a heat-sensitive ion channel. Therefore we studied to what extent heat-evoked currents in nociceptive dorsal root ganglion (DRG) neurons can be attributed to the activation of native vanilloid receptors. Heat-evoked currents were investigated in 89 neurons acutely dissociated from adult rat DRGs as models for their own terminals using the whole cell patch-clamp technique. Locally applied heated extracellular solution (effective temperature ∼53°C) rapidly activated reversible and reproducible inward currents in 80% (62/80) of small neurons (≤32.5 μm), but in none of nine large neurons ( P < 0.001, χ2 test). Heat and capsaicin sensitivity were significantly coexpressed in this subpopulation of small DRG neurons ( P < 0.001, χ2 test). Heat-evoked currents were accompanied by an increase of membrane conductance (320 ± 115%; mean ± SE, n = 7), had a reversal potential of 5 ± 2 mV ( n = 5), which did not differ from that of capsaicin-induced currents in the same neurons (4 ± 3 mV), and were carried at least by Na+ and Ca2+(pCa2+ > pNa+). These observations are consistent with the opening of temperature-operated nonselective cation channels. The duration of action potentials was significantly higher in heat-sensitive (10–90% decay time: 4.45 ± 0.39 ms, n = 12) compared with heat-insensitive neurons (2.18 ± 0.19 ms, n = 6; P< 0.005, Student's t-test), due to an inflection in the repolarizing phase. This property as well as capsaicin sensitivity and small cell size are characteristics of nociceptive DRG neurons. When coadministered with heat stimuli, the competitive VR antagonist capsazepine (1 μM to 1 mM) significantly reduced heat-evoked currents in a dose-dependent manner (IC50 13 μM, Hill slope −0.58, maximum effect 75%). Preincubation for 12–15 s shifted the IC50 by ∼0.5 log10 units to an estimated IC50 of ∼4 μM. The noncompetitive VR antagonist ruthenium red (5 μM) significantly reduced heat-evoked currents by 33 ± 6%. The effects of both VR antagonists were rapidly reversible. Our results provide evidence for a specific activation of native VRs in nociceptive primary sensory neurons by noxious heat. The major proportion of the rapid heat-evoked currents can be attributed to the activation of these temperature-operated channels, and noxious heat may be the signal detected by VRs under physiological conditions.
19
Li, Y., and C. Owyang. "Somatostatin inhibits pancreatic enzyme secretion at a central vagal site." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 2 (August 1, 1993): G251—G257. http://dx.doi.org/10.1152/ajpgi.1993.265.2.g251.
Full textAbstract:
The mechanisms and site of action of somatostatin-induced inhibition of pancreatic enzyme secretion were investigated using different stimulants of pancreatic secretion acting on different sites in anesthetized rats. Administration of graded doses of somatostatin-14 resulted in a dose-related inhibition of pancreatic protein secretion evoked by 2-deoxy-D-glucose, a central vagal stimulant that acts by stimulating the dorsal vagal nuclei. The lowest effective dose of somatostatin-14 was 1.0 microgram.kg-1 x h-1; maximal effective dose was 25 micrograms.kg-1 x h-1, which resulted in complete inhibition of protein output. Similarly, somatostatin-14 at a dose of 25 micrograms.kg-1 x h-1 also completely inhibited pancreatic protein secretion in response to a physiological concentration of cholecystokinin octapeptide (CCK-8), which acts via a vagal afferent pathway. In contrast, pancreatic protein outputs evoked by bethanechol, which directly stimulates pancreatic muscarinic receptors, or electrical stimulation of the vagal trunk, which activates the vagal efferent pathway, were unaffected by somatostatin-14. In separate studies, we demonstrated that perivagal treatment with the sensory neurotoxin capsaicin impaired pancreatic responses to CCK-8 but had no effect on the inhibitory action of somatostatin-14 on pancreatic secretion evoked by 2-deoxy-D-glucose, ruling out an effect of somatostatin on the vagal afferent pathway. Similarly we also demonstrated that perineural capsaicin treatment of the celiac-superior mesenteric ganglia did not affect the inhibitory action of somatostatin. These findings indicate that somatostatin inhibits 2-deoxy-D-glucose- and CCK-8-evoked pancreatic enzyme secretion via a vagal pathway.(ABSTRACT TRUNCATED AT 250 WORDS)
20
Fukumoto, Satoshi, Makoto Tatewaki, Tadanori Yamada, Mineko Fujimiya, Chris Mantyh, Miranda Voss, Steve Eubanks, Mary Harris, Theodore N. Pappas, and Toku Takahashi. "Short-chain fatty acids stimulate colonic transit via intraluminal 5-HT release in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 284, no. 5 (May 1, 2003): R1269—R1276. http://dx.doi.org/10.1152/ajpregu.00442.2002.
Full textAbstract:
We studied whether physiological concentration of short-chain fatty acids (SCFAs) affects colonic transit and colonic motility in conscious rats. Intraluminal administration of SCFAs (100–200 mM) into the proximal colon significantly accelerated colonic transit. The stimulatory effect of SCFAs on colonic transit was abolished by perivagal capsaicin treatment, atropine, hexamethonium, and vagotomy, but not by guanethidine. The stimulatory effect of SCFAs on colonic transit was also abolished by intraluminal pretreatment with lidocaine and a 5-hydroxytryptamine (HT)3 receptor antagonist. Intraluminal administration of SCFAs provoked contractions at the proximal colon, which migrated to the mid- and distal colon. SCFAs caused a significant increase in the luminal concentration of 5-HT of the vascularly isolated and luminally perfused rat colon ex vivo. It is suggested that the release of 5-HT from enterochromaffin cells in response to SCFAs stimulates 5-HT3 receptors located on the vagal sensory fibers. The sensory information is transferred to the vagal efferent and stimulates the release of acetylcholine from the colonic myenteric plexus, resulting in muscle contraction.
21
Li, Ying, Jinxia Zhu, and Chung Owyang. "Electrical physiological evidence for highand low-affinity vagal CCK-A receptors." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 2 (August 1, 1999): G469—G477. http://dx.doi.org/10.1152/ajpgi.1999.277.2.g469.
Full textAbstract:
We have demonstrated that under physiological conditions CCK acts through vagal high-affinity CCK-A receptors to mediate pancreatic secretion. In this study, we evaluated the vagal afferent response to endogenous CCK in rats and defined the CCK-receptor affinity states and the vagal-receptive field responsive to CCK stimulation using electrophysiological studies. Experiments were performed on anesthetized rats prepared with bile-pancreatic fistula. Plasma CCK levels were elevated by diverting bile-pancreatic juice (BPJ). The single-unit discharge of sensory neurons supplying the gastrointestinal tract was recorded from the nodose ganglia. All units studied were either silent or they had a very low resting discharge frequency. Thirty-two single units were studied extensively; seven were shown to be stimulated by diversion of BPJ (2.6 ± 2 impulses/min at basal to 40 ± 12 impulses/min after diversion). Acute subdiaphragmatic vagotomy or perivagal capsaicin treatment abolished the response. The CCK-A-receptor antagonist CR-1409, but not the CCK-B antagonist L-365260, blocked the vagal response to endogenous CCK stimulation. Infusion of the low-affinity CCK-receptor antagonist CCK-JMV-180 completely blocked the vagal afferent response to the diversion of BPJ in three of seven rats tested but had no effect on the response in the remaining four. In a separate study, we demonstrated that gastric, celiac, or hepatic branch vagotomy abolished the response in different subgroups of neurons. In conclusion, under physiological conditions, CCK acts on both high- and low-affinity CCK-A receptors present on distinct vagal afferent fibers. The vagal CCK-receptor field includes the regions innervated by the gastric, celiac, and hepatic vagal branches. This study provides electrophysiological evidence that vagal CCK receptors are present on the vagal gastric, celiac, and hepatic branches and may occur in high- and low-affinity states.
22
Macdonald, W. A., O. B. Nielsen, and T. Clausen. "Effects of calcitonin gene-related peptide on rat soleus muscle excitability: mechanisms and physiological significance." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 4 (October 2008): R1214—R1223. http://dx.doi.org/10.1152/ajpregu.00893.2007.
Full textAbstract:
Intense exercise causes a large loss of K+ from contracting muscles. The ensuing elevation of extracellular K+ ([K+]o) has been suggested to cause fatigue by depressing muscle fiber excitability. In isolated muscles, however, repeated contractions confer some protection against this effect of elevated K+. We hypothesize that this excitation-induced force-recovery is related to the release of the neuropeptide calcitonin gene-related peptide (CGRP), which stimulates the muscular Na+-K+ pumps. Using the specific CGRP antagonist CGRP-(8-37), we evaluated the role of CGRP in the excitation-induced force recovery and examined possible mechanisms. Intact rat soleus muscles were stimulated to evoke short tetani at regular intervals. Increasing extracellular K+ ([K+]o) from 4 to 11 mM decreased force to ∼20% of initial force ( P < 0.001). Addition of exogenous CGRP (10−9 M), release of endogenous CGRP with capsaicin, or repeated electrical stimulation recovered force to 50–70% of initial force ( P < 0.001). In all cases, force recovery could be almost completely suppressed by CGRP-(8-37). At 11 mM [K+]o, CGRP (10−8 M) did not alter resting membrane potential or conductance but significantly improved action potentials ( P < 0.001) and increased the proportion of excitable fibers from 32 to 70% ( P < 0.001). CGRP was shown to induce substantial force recovery with only modest Na+-K+ pump stimulation. We conclude that the excitation-induced force recovery is caused by a recovery of excitability, induced by local release of CGRP. The data suggest that the recovery of excitability partly was induced by Na+-K+ pump stimulation and partly by altering Na+ channel function.
23
Büchner, Kai, Jana Haagen, Ashtri Sastrosubroto, Roland Kerpes, Jessica Freiherr, and Thomas Becker. "Trigeminal Stimulus Menthol Masks Bitter Off-Flavor of Artificial Sweetener Acesulfame-K." Foods 11, no. 18 (September 6, 2022): 2734. http://dx.doi.org/10.3390/foods11182734.
Full textAbstract:
Consumer health concerns and regulatory policies lead to a growing demand for sugar-sweetened beverage alternatives. A reduced energy content can be achieved using artificial sweeteners, which often also convey a metallic or bitter off-flavor. Therefore, the alteration of sweetness perception and masking of potential off-flavors are paramount for improving sweet beverages. Trigeminal stimuli, such as capsaicin (spicy) or menthol (cooling), have been used to influence taste perception in food items, although their use in beverages has not yet been systematically investigated. Here, the influence of menthol on sweetness perception in an aqueous solution is examined both on the sensory and psychophysiological level. The addition of menthol had no sensory effect on sweetness perception; however, psychophysiological measurements suggest a boost in the physiological response to cold perception through the addition of sugar. Moreover, menthol addition shifted the recognition threshold of unpleasant bitterness of the sweetener acesulfame-K from 21.35 to 36.93 mg/L, masking the off-flavor. These findings illuminate the complexity of trigeminal perception influences on taste. Further investigation of these effects can render trigeminal stimuli an effective tool to enhance beverage aroma and flavor.
24
Lammers, JW, PJ Barnes, and KF Chung. "Nonadrenergic, noncholinergic airway inhibitory nerves." European Respiratory Journal 5, no. 2 (February 1, 1992): 239–46. http://dx.doi.org/10.1183/09031936.93.05020239.
Full textAbstract:
Nonadrenergic, noncholinergic (NANC) nerves, which cause relaxation of airway smooth muscle, have been described in several species including man. Stimulation of efferent vagus nerves during cholinergic and adrenergic blockade induces a pronounced bronchodilation in the cat. In more recent studies in man, capsaicin inhalation or mechanical irritation of the larynx, under conditions of cholinergic and adrenergic blockade, have been shown to cause a transient bronchodilator response. There is some evidence that neuropeptides such as vasointestinal peptide (VIP) or peptide histidine methionine (PHM) may be the neurotransmitter of NANC nerves, but this is not conclusive. Nitric oxide may be another neurotransmitter. In mild asthma, the NANC bronchodilator response is similar to that observed in normal subjects; on the other hand, a reduction in VIP immunoreactivity has been reported in more severe patients. The contribution of NANC dilator nerves in pathophysiological situations is not known, but their effect may be modulated during allergic responses. Use of antagonists or inhibitors of putative neurotransmitters, and molecular biological techniques will be useful in defining both the physiological and pathophysiological roles of NANC inhibitory nerves in the airways.
25
Ni, Dan, and Lu-Yuan Lee. "Effect of increasing temperature on TRPV1-mediated responses in isolated rat pulmonary sensory neurons." American Journal of Physiology-Lung Cellular and Molecular Physiology 294, no. 3 (March 2008): L563—L571. http://dx.doi.org/10.1152/ajplung.00336.2007.
Full textAbstract:
Hyperthermia has been shown to sensitize vagal pulmonary C-fibers in anesthetized rats. However, it was not clear whether the effect was due to a direct action of hyperthermia on these sensory neurons. To answer this question, we carried out this study to determine the effect of increasing temperature on the responses to various chemical stimuli in isolated nodose and jugular ganglion neurons innervating the rat lungs. In the whole cell perforated patch-clamp study, when the temperature was increased from normal (∼36°C) to hyperthermic (∼40.6°C) level of the rat body temperature, the inward currents evoked by capsaicin, a selective activator of the transient receptor potential vanilloid type 1 (TRPV1), and 2-aminoethoxydiphenyl borate (2-APB), a nonselective activator of TRPV1–3 receptors, were both significantly increased. This potentiating effect was clearly present even at a moderate level of hyperthermia (∼39°C). However, only the slow, sustained component of acid-evoked current mediated through the TRPV1 receptor was potentiated by hyperthermia, whereas the rapid, transient component was inhibited. In contrast, the currents evoked by adenosine 5′-triphosphate and acetylcholine, neither of which is known to activate the TRPV1 channel, did not increase when the same temperature elevation was applied. Furthermore, the hyperthermia-induced potentiation of the cell response to 2-APB was significantly attenuated by either capsazepine or AMG 9810, selective TRPV1 antagonists. In conclusion, increasing temperature within the physiological range exerts a potentiating effect on the response to TRPV1 activators in these neurons, which is probably mediated through a positive interaction between hyperthermia and these chemical activators at the TRPV1 channel.
26
Braga. Feitoza, Luis Felipe Barbosa, Hans Christian Muller, Tom Williams, and James Drouillard. "PSII-3 Effect of molasses-based block supplementation on cattle fed endophyte-infected Tall Fescue (Festuca arundinacea) seed." Journal of Animal Science 97, Supplement_2 (July 2019): 227–28. http://dx.doi.org/10.1093/jas/skz122.400.
Full textAbstract:
Abstract Ergot-alkaloid toxicosis induces persistent vasoconstriction in cattle, interfering with efficient thermoregulation. Our objective was to evaluate impact of cooked molasses-based block supplements (MBS) on performance and physiological measurements in cattle fed ergot-containing Tall Fescue seed (TFS). Crossbred steers (n = 95; 287 ± 6.4 kg) were blocked by body weight, randomly assigned to individual indoor feeding pens and treatments consisting of: Negative Control (NC; prairie hay only); Positive Control (PC; hay plus TFS); and molasses block treatments fed hay and TFS with ad libitum access to a 38% protein block (CB); 38% protein block containing 0.3% crystalline menthol (MB); or a 38% protein block containing a proprietary blend of mannan oligosaccharide and capsaicin (AB). The TFS was mixed with molasses (9:1), and amount fed was increased gradually at 3-d intervals from 45 to 520 g/animal daily by day 42. Temperature differential between ocular conjunctiva and ear tip (ΔT) was determined weekly using thermographic imaging. Coccigeal vein diameter (CVD) was measured with Doppler ultrasound imaging (DU) on days 63 and 84. Data were analyzed as mixed models with block as a random effect and treatment, time, and treatment by time interaction as fixed effects. Block intakes did not differ among MBS treatments (P > 0.05). Cattle fed MBS had greater ADG, DMI, gain:feed (P < 0.01) compared to NC and PC. For the second half of the study MBS treatments had lower ΔT (P < 0.05). Supplementing cooked molasses-based block supplements low-moisture molasses block can improve performance and potentially enhance peripheral blood irrigation in cattle consuming ergot-infested feeds.
27
Donald, J. A., J. E. O'Shea, and H. B. Lillywhite. "Somatostatin and innervation of the heart of the snake Elaphe obsoleta." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 4 (April 1, 1990): R1001—R1007. http://dx.doi.org/10.1152/ajpregu.1990.258.4.r1001.
Full textAbstract:
The innervation of the heart of the snake Elaphe obsoleta was examined with peptide immunohistochemistry, glyoxylic acid-induced catecholamine fluorescence, and in vitro physiological preparations. Snakes were anesthetized with Nembutal. Many somatostatin (SOM)-like immunoreactive (LI) axons were observed in the sinus venosus, atria, and ventricle. Cell bodies with SOM-LI were found in the intracardiac nerve trunks of the sinus venosus, the interatrial septum, and the atrioventricular region. The SOM-LI axons and cell bodies were not affected by 6-hydroxy-dopamine and capsaicin. They are probably intrinsic parasympathetic neurons. Adrenergic, neuropeptide Y-LI, substance P-LI, and calcitonin gene-related peptide-LI axons were found in the sinus venosus, atria, and ventricle. In spontaneously beating sinoatrial or electrically driven atrial preparations, applied SOM (6 x 10(-9) M and 6 x 10(-8) M) decreased the force of atrial contraction and/or the rate of beating. The effects of SOM were tachyphylactic. SOM had no effect on the force of contraction of the driven ventricle. Stimulation of the left and right vagus nerves elicited negative chronotropic and inotropic responses followed by poststimulus positive inotropic and chronotropic responses. Atropine abolished the inhibition, and bretylium abolished the excitation. After cholinergic and adrenergic blockade, high-frequency vagal nerve stimulation had no effect on heart rate and the force of contraction. Thus, although there is an extensive distribution of intrinsic SOM-LI neurons in the heart and although applied SOM is a potent inhibitor of rate and force, SOM in the vagal neurons does not appear to act as a direct inhibitory transmitter to the cardiac muscle or pacemaker cells.
28
García-López, Niño-Medina, Olivares-Sáenz, Lira-Saldivar, Barriga-Castro, Vázquez-Alvarado, Rodríguez-Salinas, and Zavala-García. "Foliar Application of Zinc Oxide Nanoparticles and Zinc Sulfate Boosts the Content of Bioactive Compounds in Habanero Peppers." Plants 8, no. 8 (July 30, 2019): 254. http://dx.doi.org/10.3390/plants8080254.
Full textAbstract:
The physiological responses of habanero pepper plants (Capsicum chinense Jacq.) to foliar applications of zinc sulphate and zinc nano-fertilizer were evaluated in greenhouse trials. The effect of the supplement on fruit quality of habanero pepper was particularly observed. Habanero pepper plants were grown to maturity, and during the main stages of phenological development, they were treated with foliar applications of Zn at concentrations of 1000 and 2000 mg L−1 in the form of zinc sulfate (ZnSO4) and zinc oxide nanoparticles (ZnO NPs). Additional Zn was not supplied to the control treatment plants. ZnO NPs at a concentration of 1000 mg L−1 positively affected plant height, stem diameter, and chlorophyll content, and increased fruit yield and biomass accumulation compared to control and ZnSO4 treatments. ZnO NPs at 2000 mg L−1 negatively affected plant growth but significantly increased fruit quality, capsaicin content by 19.3%, dihydrocapsaicin by 10.9%, and Scoville Heat Units by 16.4%. In addition, at 2000 ZnO NPs mg L−1 also increased content of total phenols and total flavonoids (soluble + bound) in fruits (14.50% and 26.9%, respectively), which resulted in higher antioxidant capacity in ABTS (2,2′azino-bis(3-ethylbenzothiazoline-6-sulfonic acid)), DPPH (2,2-diphenyl-1-picrylhydrazyl), and FRAP (ferric reducing antioxidant power) (15.4%, 31.8%, and 20.5%, respectively). These results indicate that application of ZnO NPs could be employed in habanero pepper production to improve yield, quality, and nutraceutical properties of fruits.
29
Gibbs, J. L., and K. M. Hargreaves. "Neuropeptide Y Y1 Receptor Effects on Pulpal Nociceptors." Journal of Dental Research 87, no. 10 (October 2008): 948–52. http://dx.doi.org/10.1177/154405910808701008.
Full textAbstract:
Neuropeptide Y (NPY) is an important modulatory neuropeptide that regulates several physiological systems, including the activity of sensory neurons. We evaluated whether activation of the NPY Y1 receptor could modulate the activity of capsaicin-sensitive nociceptors in trigeminal ganglia and dental pulp. We tested this hypothesis by measuring capsaicin-stimulated calcitonin gene-related peptide release (CGRP) as a measure of nociceptor activity. Capsaicin-evoked CGRP release was inhibited by 50% (p < 0.05) in trigeminal ganglia and by 26% (p < 0.05) in dental pulp when tissues were pre-treated with [Leu31,Pro34]NPY. The Y1 receptor was found to co-localize with the capsaicin receptor TRPV1 in trigeminal ganglia. These results demonstrate that activation of the Y1 receptor results in the inhibition of the activity of capsaicin-sensitive nociceptors in the trigeminal ganglia and dental pulp. These findings are relevant to the physiological modulation of dental nociceptors by endogenous NPY and demonstrate an important novel analgesic target for the treatment of dental pain.
30
Lu, Yuan-Xu, and Chung Owyang. "Duodenal acid-induced gastric relaxation is mediated by multiple pathways." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 6 (June 1, 1999): G1501—G1506. http://dx.doi.org/10.1152/ajpgi.1999.276.6.g1501.
Full textAbstract:
In this study, we used an in vivo anesthetized rat model to investigate the mechanisms responsible for duodenal acid-induced inhibition of gastric motility. Intraduodenal infusion of HCl produced a rate-dependent decrease in intragastric pressure. Infusion of HCl at 2 ml/h produced a physiological plasma secretin level and elicited a decrease in intragastric pressure of 3.0 ± 0.2 cmH20. Infusion of rabbit secretin antiserum reduced the acid-induced inhibition of gastric motility by 85 ± 5%, suggesting mediation mainly by endogenous secretin. Administration of the cholecystokinin (CCK)-A antagonist MK-329 caused only a modest 10 ± 3% reduction in gastric relaxation, whereas the serotonin antagonist ICS-205930 had no effect. In contrast, immunoneutralization with the secretin antibody caused only a 15% reduction in the relaxation evoked by a higher rate of HCl infusion (3 ml/h), whereas MK-329 and ICS-205930 caused a 20 ± 4% reduction and no reduction, respectively. Bilateral truncal vagotomy or perivagal application of capsaicin completely abolished gastric relaxation in response to low rates (1–2 ml/h) of 0.1 N HCl infusion but only partially affected gastric relaxation in response to a higher infusion rate (3 ml/h). These observations indicate that multiple pathways mediate the duodenal acid-induced inhibition of gastric motility. At low rates of HCl infusion, gastric relaxation is mediated primarily by endogenous secretin, which acts through vagal afferent pathways. At higher rates of HCl infusion, gastric relaxation is mediated by endogenous secretin, CCK, and possibly by the direct action of HCl on vagal afferent pathways or yet unidentified neuropathways.
31
Mazda, Takayuki, Hiroshi Yamamoto, Masaki Fujimura, and Mineko Fujimiya. "Gastric distension-induced release of 5-HT stimulates c-fos expression in specific brain nuclei via 5-HT3 receptors in conscious rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 1 (July 2004): G228—G235. http://dx.doi.org/10.1152/ajpgi.00373.2003.
Full textAbstract:
We examined c- fos expression in specific brain nuclei in response to gastric distension and investigated whether 5-HT released from enterochromaffin (EC) cells was involved in this response. The role of 5-HT3 receptors in this mechanism was also addressed. Release of 5-HT was examined in an ex vivo-perfused stomach model, whereas c- fos expression in brain nuclei induced by gastric distension was examined in a freely moving conscious rat model. Physiological levels of gastric distension stimulated the vascular release of 5-HT more than luminal release of 5-HT, and induced c- fos expression in the nucleus of the solitary tract (NTS), area postrema (AP), paraventricular nucleus (PVN), and supraoptic nucleus (SON). The c- fos expression in all these brain nuclei was blocked by truncal vagotomy as well as by perivagal capsaicin treatment, suggesting that vagal afferent pathways may mediate this response. Intravenous injection of 5-HT3 receptor antagonist granisetron blocked c- fos expression in all brain nuclei examined, although intracerebroventricular injection of granisetron had no effect, suggesting that 5-HT released from the stomach may activate 5-HT3 receptors located in the peripheral vagal afferent nerve terminals and then induce brain c- fos expression. c- fos Positive cells in the NTS were labeled with retrograde tracer fluorogold injected in the PVN, suggesting that neurons in the NTS activated by gastric distension project axons to the PVN. The present results suggest that gastric distension stimulates 5-HT release from the EC cells and the released 5-HT may activate 5-HT3 receptors located on the vagal afferent nerve terminals in the gastric wall leading to neuron activation in the NTS and AP and subsequent activation of neurons in the PVN and SON.
32
Szabados, Tamara, Kamilla Gömöri, Laura Pálvölgyi, Anikó Görbe, István Baczkó, Zsuzsanna Helyes, Gábor Jancsó, Péter Ferdinandy, and Péter Bencsik. "Capsaicin-Sensitive Sensory Nerves and the TRPV1 Ion Channel in Cardiac Physiology and Pathologies." International Journal of Molecular Sciences 21, no. 12 (June 23, 2020): 4472. http://dx.doi.org/10.3390/ijms21124472.
Full textAbstract:
Cardiovascular diseases, including coronary artery disease, ischemic heart diseases such as acute myocardial infarction and postischemic heart failure, heart failure of other etiologies, and cardiac arrhythmias, belong to the leading causes of death. Activation of capsaicin-sensitive sensory nerves by the transient receptor potential vanilloid 1 (TRPV1) capsaicin receptor and other receptors, as well as neuropeptide mediators released from them upon stimulation, play important physiological regulatory roles. Capsaicin-sensitive sensory nerves also contribute to the development and progression of some cardiac diseases, as well as to mechanisms of endogenous stress adaptation leading to cardioprotection. In this review, we summarize the role of capsaicin-sensitive afferents and the TRPV1 ion channel in physiological and pathophysiological functions of the heart based mainly on experimental results and show their diagnostic or therapeutic potentials. Although the actions of several other channels or receptors expressed on cardiac sensory afferents and the effects of TRPV1 channel activation on different non-neural cell types in the heart are not precisely known, most data suggest that stimulation of the TRPV1-expressing sensory nerves or stimulation/overexpression of TRPV1 channels have beneficial effects in cardiac diseases.
33
White, C. B., A. M. Roberts, and I. G. Joshua. "Arteriolar dilation mediated by capsaicin and calcitonin gene-related peptide in rats." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1411—H1415. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1411.
Full textAbstract:
In addition to altering vascular tone by stimulating primary afferent nerves and acting through reflex pathways, capsaicin acts locally. We examined effects of topically applied capsaicin on arteriolar diameter in striated muscle and tested the hypothesis that capsaicin can alter microvascular tone by releasing substance P (SP) or calcitonin gene-related peptide (CGRP). In anesthetized rats, the right cremaster muscle was exposed and suspended in a tissue bath filled with a physiological salt solution. Diameters of third-order arterioles were displayed and measured using in vivo video microscopy. In 17 of 20 rats, addition of capsaicin (3 x 10(-7) M) to the bath dilated arterioles (85 +/- 14% above control). Failure of a second administration of capsaicin to produce a sustained dilation in 6 of 7 arterioles that had previously dilated to capsaicin is consistent with the hypothesis that this agent causes depletion of an endogenous vasodilator. Pretreatment with an SP inhibitor did not alter capsaicin-induced dilation. CGRP (1 x 10(-10) to 2 x 10(-8) M) caused dilation similar to that caused by capsaicin. Pretreatment with a CGRP inhibitor to the bath prevented capsaicin-induced dilation, but not constriction. These results suggest that capsaicin can dilate microvessels by releasing CGRP, which can modulate tone.
34
Pfanzagl, Beatrix, Victor F. Zevallos, Detlef Schuppan, Roswitha Pfragner, and Erika Jensen-Jarolim. "Histamine causes influx via T-type voltage-gated calcium channels in an enterochromaffin tumor cell line: potential therapeutic target in adverse food reactions." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 2 (February 1, 2019): G291—G303. http://dx.doi.org/10.1152/ajpgi.00261.2018.
Full textAbstract:
The P-STS human ileal neuroendocrine tumor cells, as a model for gut enterochromaffin cells, are strongly and synergistically activated by histamine plus acetylcholine (ACh), presumably via histamine 4 receptors, and weakly activated by histamine alone. Sensing these signals, enterochromaffin cells could participate in intestinal intolerance or allergic reactions to food constituents associated with elevated histamine levels. In this study we aimed to analyze the underlying molecular mechanisms. Inhibition by mepyramine and mibefradil indicated that histamine alone caused a rise in intracellular calcium concentration ([Ca2+]i) via histamine 1 receptors involving T-type voltage-gated calcium channels (VGCCs). Sensitivity to histamine was enhanced by pretreatment with the inflammatory cytokine tumor necrosis factor-α (TNF-α). In accordance with the relief it offers some inflammatory bowel disease patients, otilonium bromide, a gut-impermeable inhibitor of T-type (and L-type) VGCCs and muscarinic ACh receptors, efficiently inhibited the [Ca2+]i responses induced by histamine plus ACh or by histamine alone in P-STS cells. It will take clinical studies to show whether otilonium bromide has promise for the treatment of adverse food reactions. The cells did not react to the nutrient constituents glutamate, capsaicin, cinnamaldehyde, or amylase-trypsin inhibitors and the transient receptor potential channel vanilloid 4 agonist GSK-1016790A. The bacterial product butyrate evoked a rise in [Ca2+]i only when added together with ACh. Lipopolysaccharide had no effect on [Ca2+]i despite the presence of Toll-like receptor 4 protein. Our results indicate that inflammatory conditions with elevated levels of TNF-α might enhance histamine-induced serotonin release from intestinal neuroendocrine cells. NEW & NOTEWORTHY We show that histamine synergistically enhances the intracellular calcium response to the physiological agonist acetylcholine in human ileal enterochromaffin tumor cells. This synergistic activation and cell activation by histamine alone largely depend on T-type voltage-gated calcium channels and are inhibited by the antispasmodic otilonium bromide. The cells showed no response to wheat amylase-trypsin inhibitors, suggesting that enterochromaffin cells are not directly involved in nongluten wheat sensitivity.
35
Bowles, W. R., C. M. Flores, D. L. Jackson, and K. M. Hargreaves. "β2-Adrenoceptor Regulation of CGRP Release from Capsaicin-sensitive Neurons." Journal of Dental Research 82, no. 4 (April 2003): 308–11. http://dx.doi.org/10.1177/154405910308200413.
Full textAbstract:
Previous studies have suggested that neurotransmitter substances from the sympatho-adrenomedullary system regulate pulpal blood flow (PBF), in part, by the inhibition of vasoactive neuropeptide release from pulpal sensory neurons. However, no study has evaluated the role of β-adrenoceptors. We evaluated the hypothesis that activation of β-adrenoceptors inhibits immunoreactive calcitonin gene-related peptide (iCGRP) release from capsaicin-sensitive nociceptive neurons via in vitro superfusion of bovine dental pulp. Either norepinephrine or epinephrine inhibited capsaicin-evoked iCGRP. The norepinephrine effect was blocked by the selective β2-adrenoceptor antagonist, ICI 118,551, but not by pre-treatment with the selective β1-adrenoceptor antagonist, atenolol. In addition, application of albuterol, a selective β2-adrenoceptor agonist, significantly blocked capsaicin-evoked release of iCGRP. Collectively, these studies demonstrate that activation of β2-adrenoceptors in dental pulp significantly reduces exocytosis of neuropeptides from capsaicin-sensitive nociceptors. This effect may have physiologic significance in regulating PBF. Moreover, since capsaicin selectively activates nociceptors, β2-adrenoceptor agonists may have clinical utility as peripherally acting therapeutics for dental pain and inflammation.
36
Wang, Junzheng, Zixing Gao, Tao Sun, Wenxian Huang, Yuanjie Jia, Xiaojing Li, Zhi Zhang, and Xiaohui Hu. "Preharvest Reduction in Nutrient Solution Supply of Pepper (Capsicum annuum L.) Contributes to Improve Fruit Quality and Fertilizer Efficiency While Stabilising Yields." Agronomy 12, no. 12 (November 29, 2022): 3004. http://dx.doi.org/10.3390/agronomy12123004.
Full textAbstract:
Optimising fertilisation is an important part of maximising vegetable yield and quality whilst minimising environmental hazards. An accurate and efficient scheme of irrigation and fertiliser based on plants’ nutrient requirements at different growth stages is essential for the effective intensive production of greenhouse pepper (Capsicum annuum L.). In this study, the effects of reducing fertilisation rate by 20%, 40%, 60% and 80% from the day 6 to day 0 before harvest for each layer of peppers on growth, yield, quality and nutrient utilisation were evaluated. The results showed that the morphological indicators (plant height and stem diameter) and biomass of plants decreased gradually with the increase in fertiliser reduction rate. Compared with control (CK) plants, the 20–40% reduction in fertiliser application rate did not cause a significant decrease in biomass and stem diameter but significantly increased the accumulation of N (13.52–15.73%), P (23.09% in 20% reducted-treatment) and K (13.22–14.21%) elements in plants. The 20–80% reduction in fertiliser application before harvest had no significant effects on the nutrient agronomic efficiency of N, P and K elements. However, it decreased the physiological nutrient efficiency and significantly improved the nutrient harvest index of N, P and K. Appropriate reduction in fertiliser application significantly increased the nutrient recovery efficiency (20–40% reduction) and nutrient partial-factor productivity (40% reduction) of N (3.35–6.00% and 12.87%), P (2.47–2.92% and 14.01%) and K (7.49–15.68% and 14.01%), respectively. Furthermore, reducing the fertilisation rate by 20–40% before each harvest had a certain positive effect on the C and N metabolism of pepper leaves and fruits. In particular, the activities of N metabolism-related enzymes (nitrate reductase, nitrite reductase, glutamine synthase, glutamate synthase and glutamate dehydrogenase) and C metabolism-related enzymes (sucrose phosphate synthase, sucrose synthetase, acid invertase and neutral invertase) in leaves and fruits did not significantly different or significantly increased compared with those in CK plants. The results of the representative aromatic substance contents in the fruit screened by the random forest model showed that compared with the CK plants, reducing the fertiliser application by 20–40% before harvest significantly increased the content of capsaicin and main flavour substances in the fruit on the basis of stable yield. In summary, in the process of pepper substrate cultivation, reducing the application of nutrients by 40% from the day 6 to day 0 before each harvest could result in stable yield and quality improvement of the pepper. These results have important implications for institutional precision fertilisation programs and the improvement of the agroecological environment.
37
von Ah Morano, Ana Elisa, Camila S. Padilha, Vinicius Aparecido Matos Soares, Fabiana Andrade Machado, Peter Hofmann, Fabrício E. Rossi, and Fábio Santos Lira. "Capsaicin Analogue Supplementation Does Not Improve 10 km Running Time-Trial Performance in Male Amateur Athletes: A Randomized, Crossover, Double-Blind and Placebo-Controlled Study." Nutrients 13, no. 1 (December 24, 2020): 34. http://dx.doi.org/10.3390/nu13010034.
Full textAbstract:
Background: To investigate the acute effects of a capsaicin analogue supplement on 10 km time-trial performance and physiological responses in amateur athletes. Methods: Twenty-one participants (age = 29.3 ± 5.5 years, weight 74.2 ± 11.3 kg, height 176.0 ± 0.0 cm, fat mass 12.7 ± 3.8%, V˙O2max 62.7 ± 8.4 mL·k−1·min−1), completed two randomized, double-blind trials: capsaicin analogue condition (Capsiate (CAP) = 24 mg) or a placebo (PLA) condition. The participants consumed two doses of 12 mg of CAP or PLA capsule 45 min before and immediately at the start of each trial. The time required to complete 10 km, lactate concentration, maximum heart rate (HRpeak), and rating of perceived exertion (RPE) were recorded. Results: The 10 km time-trial performance (CAP = 45.07 ± 6.41 min vs. PLA = 45.13 ± 6.73, p = 0.828) was not statistically significantly different between conditions. No statistically significant differences between conditions were detected for lactate concentration (p = 0.507), HRpeak (p = 0.897) and RPE (p = 0.517). Conclusion: Two doses of a 12 mg Capsaicin analogue supplement did not improve performance and physiological responses in a 10 km running time-trial in amateur athletes.
38
De Sanctis, G. T., E. M. App, J. K. Trask, B. I. De Sanctis, J. E. Remmers, F. H. Green, S. F. Man, and M. King. "Resorptive clearance and transepithelial potential difference in capsaicin-treated F344 rats." Journal of Applied Physiology 68, no. 5 (May 1, 1990): 1826–32. http://dx.doi.org/10.1152/jappl.1990.68.5.1826.
Full textAbstract:
The long-term effects of substance P (SP) depletion on epithelial integrity were assessed by measurements of airway transepithelial potential difference (PD) and resorptive clearance. Both techniques are highly sensitive to differences in epithelial permeability. PD (mV) was assayed with a KCl-saturated agar bridge technique in the lower trachea of Fischer 344 rats depleted of SP by neonatal capsaicin treatment. Capsaicin treatment is known to ablate a subpopulation of primary afferent fibers containing SP. Resorptive clearance (clearance in 1 h) was measured with 99mTc-labeled diethylenetriaminepentaacetic acid administered as a 100-microliters (100 microCi) bolus. Depletion of SP by neonatal treatment with capsaicin resulted in a highly significant increase in resorptive clearance (P less than 0.001). There was also a significant difference in PD in the lower trachea, the values being less negative for the capsaicin-treated rats (P less than 0.005). The increase in resorptive clearance may reflect the leakiness of the epithelial membrane, as also suggested by the decrease in PD. Aside from its known involvement as a neurotransmitter in neurogenic inflammation, SP may, under normal physiological conditions, have an additional role in the maintenance of epithelial barrier function.
39
Ewart, W. R., M. V. Jones, and M. P. Primi. "Bombesin changes excitability of rat brain stem neurons sensitive to gastric distension." American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no. 6 (June 1, 1990): G841—G847. http://dx.doi.org/10.1152/ajpgi.1990.258.6.g841.
Full textAbstract:
The responses of single neurons in the dorsal vagal complex to physiological gastric distension were investigated in anesthetized control and capsaicin-treated rats. In both groups, the responses of brain stem neurons to close arterial injection of the regulatory peptide bombesin (BBS) were studied. These experiments observed whether selective chemical deafferentation by capsaicin caused any significant change in the central representation of responses to gastric distension and peripheral BBS administration. In 43 animals a total of 49 neurons was studied, 21 of which were in rats pretreated with capsaicin. In normal animals, the majority of neurons (89%, n = 28) responded in the same manner (increase or decrease in firing rate) to gastric distension and peripheral BBS administration. Of the 21 neurons studied in capsaicin-treated rats, 76% responded in the same direction to gastric distension and BBS. Two neurons responsive to gastric distension failed to respond to BBS. There was no significant difference between the proportion of neurons responding both to gastric distension and BBS in normal and capsaicin-treated rats. Responses to both gastric distension and BBS were abolished by bilateral cervical vagotomy in both groups of rats. In these experiments, BBS apparently acted on peripheral receptors near the stomach to produce, via the vagus nerve, effects on neuronal excitability in the dorsal vagal complex. Almost all of these neurons were also responsive to activation of gastric mechanoreceptors. The responses of dorsal vagal complex neurons to gastric distension and peripheral BBS were capsaicin insensitive, which is in contrast to the action of cholecystokinin under the same conditions.
40
Zafra, Maria A., Filomena Molina, and Amadeo Puerto. "Learned flavor preferences induced by intragastric administration of rewarding nutrients: role of capsaicin-sensitive vagal afferent fibers." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 2 (August 2007): R635—R641. http://dx.doi.org/10.1152/ajpregu.00136.2007.
Full textAbstract:
Learned flavor preferences can be established after intragastric nutrient administration by two different behavioral procedures, concurrent and sequential. In a concurrent procedure, two flavored stimuli are offered separately but at the same time on a daily basis: one stimulus is paired with the simultaneous intragastric administration of partially digested food and the other with physiological saline. In sequential learning, the two stimuli are presented during alternate sessions. Neural mechanisms underlying these learning modalities have yet to be fully elucidated. The aim of this study was to examine the role of vagal afferent fibers in the visceral processing of rewarding nutrients during concurrent ( experiment 1) and sequential ( experiment 2) flavor preference learning in Wistar rats. For this purpose, capsaicin, a neurotoxin that destroys slightly myelinated or unmyelinated sensory axons, was applied to the subdiaphragmatic region of the esophagus to selectively damage most of the vagal afferent pathways that originate in the gastrointestinal system. Results showed that capsaicin [1 mg of capsaicin dissolved in 1 ml of vehicle (10% Tween 80 in oil)] blocked acquisition of concurrent but not sequential flavor preference learning. These results are interpreted in terms of a dual neurobiological system involved in processing the rewarding effects of intragastrically administered nutrients. The vagus nerve, specifically capsaicin-sensitive vagal afferent fibers, would only be essential in concurrent flavor preference learning, which requires rapid processing of visceral information.
41
Pettit, M. J., and H. D. Schwark. "Capsaicin-induced rapid receptive field reorganization in cuneate neurons." Journal of Neurophysiology 75, no. 3 (March 1, 1996): 1117–25. http://dx.doi.org/10.1152/jn.1996.75.3.1117.
Full textAbstract:
1. To determine whether activity in unmyelinated or thinly myelinated primary afferents affects the organization of cutaneous receptive fields (RFs) in the cuneate nucleus, subcutaneous injections of capsaicin were made into the RFs of cuneate neurons in anesthetized cats. The effects of capsaicin injection on RF size and position, response properties, and spontaneous firing rates were determined during single-unit recordings. 2. Subcutaneous injection of capsaicin (10% dissolved in 70% ethanol) into peripheral RFs produced rapid RF reorganization in all neurons tested (n = 20), even when the original RF remained responsive to tactile stimulation. RF reorganization was marked by the appearance of newly responsive RFs. These RFs appeared as either contiguous expansions of the original RF or as new, noncontiguous fields. Control injections of the vehicle alone never produced RF reorganization (n = 9). RF reorganization was not related to changes in spontaneous activity. 3. Following capsaicin-induced RF reorganization, subcutaneous injections of lidocaine were made into the original RFs (n = 8). These injections produced no additional RF reorganization in seven of the eight neurons, even though in each case the lidocaine injections produced at least partial blocks of responsiveness from within the original RF. 4. In approximately one-half of the neurons (9 of 20), the reorganized RFs had response properties that were different from those of the original RF. This result suggests that, for neurons in the dorsal column nuclei (DCN), physiological mechanisms that normally mask inputs and restrict RF size can give rise to response specificity. 5. The results of these experiments demonstrate that capsaicin-induced RF reorganization, which has been reported previously in ventrobasal thalamus and primary somatosensory cortex, can arise within the dorsal column-medial lemniscal system, at the level of the DCN. The present results also provide evidence that rapid RF reorganization in cuneate neurons can be produced by blockade of a subset of peripheral afferents that are sensitive to capsaicin.
42
Ali, W., A. Ahmed, and Hoda El-Gabry. "EFFECTS OF CAPSAICIN SUPPLEMENTATION ON PRODUCTIVE AND PHYSIOLOGICAL PERFORMANCE OF PEKIN DUCKS DURING SUMMER SEASON." Egyptian Journal of Nutrition and Feeds 19, no. 3 (December 1, 2016): 549–61. http://dx.doi.org/10.21608/ejnf.2016.74996.
Full text
43
Chen, Meng, and Jianguo G. Gu. "A P2X Receptor-Mediated Nociceptive Afferent Pathway to Lamina I of the Spinal Cord." Molecular Pain 1 (January 1, 2005): 1744–8069. http://dx.doi.org/10.1186/1744-8069-1-4.
Full textAbstract:
Of the six lamina regions in the dorsal horn of the spinal cord, lamina I is a major sensory region involved in nociceptive transmission under both physiological and pathological conditions. While P2X receptors have been shown to be involved in nociception, it remains unknown if P2X receptors are involved in nociceptive transmission to lamina I neurons. Using rat spinal cord slice preparations and patch-clamp recordings, we have demonstrated that the excitatory synaptic transmission between primary afferent fibers and lamina I neurons is significantly affected by ATP and α,β-methylene-ATP. The synaptic effects of them include the increases of the frequency of both miniature excitatory postsynaptic currents (mEPSCs) and spontaneous EPSCs (sEPSCs), and decreases of evoked EPSCs (eEPSCs). These effects were blocked by pyridoxalphosphate-6-azophenyl-2′, 4′-disulfonic acid (PPADS, 10 μM) and suramin (30 μM). In the neurons for which ATP and α,β-methylene-ATP had effects on mEPSCs, sEPSCs and eEPSCs, capsaicin produced similar synaptic effects. Our results indicate that P2X receptors are expressed on many afferent fibers that directly synapse to lamina I neurons. Furthermore, these P2X receptor-expressing afferent fibers are capsaicin-sensitive nociceptive afferents. Thus, this study reveals a P2X receptor-mediated nociceptive afferent pathway to lamina I of the spinal cord and provides a new insight into the nociceptive functions of P2X receptors.
44
Mizuno, Masaki, Gary A. Iwamoto, Wanpen Vongpatanasin, Jere H. Mitchell, and Scott A. Smith. "Dynamic exercise training prevents exercise pressor reflex overactivity in spontaneously hypertensive rats." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 5 (September 2015): H762—H770. http://dx.doi.org/10.1152/ajpheart.00358.2015.
Full textAbstract:
Cardiovascular responses to exercise are exaggerated in hypertension. We previously demonstrated that this heightened cardiovascular response to exercise is mediated by an abnormal skeletal muscle exercise pressor reflex (EPR) with important contributions from its mechanically and chemically sensitive components. Exercise training attenuates exercise pressor reflex function in healthy subjects as well as in heart failure rats. However, whether exercise training has similar physiological benefits in hypertension remains to be elucidated. Thus we tested the hypothesis that the EPR overactivity manifest in hypertension is mitigated by exercise training. Changes in mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) in response to muscle contraction, passive muscle stretch, and hindlimb intra-arterial capsaicin administration were examined in untrained normotensive Wistar-Kyoto rats (WKYUT; n = 6), exercise-trained WKY (WKYET; n = 7), untrained spontaneously hypertensive rats (SHRUT; n = 8), and exercise-trained SHR (SHRET; n = 7). Baseline MAP after decerebration was significantly decreased by 3 mo of wheel running in SHRET (104 ± 9 mmHg) compared with SHRUT (125 ± 10 mmHg). As previously reported, the pressor and renal sympathetic responses to muscle contraction, stretch, and capsaicin administration were significantly higher in SHRUT than WKYUT. Exercise training significantly attenuated the enhanced contraction-induced elevations in MAP (SHRUT: 53 ± 11 mmHg; SHRET: 19 ± 3 mmHg) and RSNA (SHRUT: 145 ± 32%; SHRET: 57 ± 11%). Training produced similar attenuating effects in SHR during passive stretch and capsaicin administration. These data demonstrate that the abnormally exaggerated EPR function that develops in hypertensive rats is significantly diminished by exercise training.
45
Hoover, Donald B. "Effects of capsaicin on release of substance P-like immunoreactivity and physiological parameters in isolated perfused guinea-pig heart." European Journal of Pharmacology 141, no. 3 (September 1987): 489–92. http://dx.doi.org/10.1016/0014-2999(87)90571-1.
Full text
46
Brown, Dorothy Cimino, Michael J. Iadarola, Sandra Z. Perkowski, Hardam Erin, Frances Shofer, Karai J. Laszlo, Zoltan Olah, and Andrew J. Mannes. "Physiologic and Antinociceptive Effects of Intrathecal Resiniferatoxin in a Canine Bone Cancer Model." Anesthesiology 103, no. 5 (November 1, 2005): 1052–59. http://dx.doi.org/10.1097/00000542-200511000-00020.
Full textAbstract:
Background Resiniferatoxin is a potent capsaicin analog. Intrathecal administration leads to selective, prolonged opening of the transient receptor potential V1 ion channel, which is localized mainly to C-fiber primary afferent nociceptive sensory neurons. Following work in laboratory animals, the authors explored the use of intrathecal resiniferatoxin to control spontaneous bone cancer pain in companion (pet) dogs. Methods Normal canine population: Behavioral testing was performed to establish baseline paw withdrawal latency; subsequently, general anesthesia was induced and resiniferatoxin was administered intrathecally while hemodynamic parameters were recorded. Behavior testing was repeated for 12 days after administration of resiniferatoxin. Clinical canine population: Twenty companion dogs with bone cancer pain were recruited. The animal's baseline level of discomfort and analgesic use were recorded. Resiniferatoxin was administered intrathecally and hemodynamic parameters were monitored while the dogs were under general anesthesia. Dogs were reevaluated up to 14 weeks after resiniferatoxin administration. Results Normal canine population: In the first minutes after resiniferatoxin injection, there were significant (P < 0.05) increases in mean arterial blood pressure and heart rate from baseline. Two days after injection, limb withdrawal latencies increased to the point of cutoff in the dogs that received at least 1.2 microg/kg resiniferatoxin. Clinical canine population: From baseline, there were significant (P < 0.05) increases in mean arterial blood pressure and heart rate after resiniferatoxin injection. Comfort scores were significantly improved at 2, 6, 10, and 14 weeks after resiniferatoxin administration (P < 0.0001). There was decreased or discontinued use of supplemental analgesics in 67% of the dogs 2 weeks after resiniferatoxin administration. Conclusions Intrathecal resiniferatoxin elicits transient hemodynamic effects. In controls, a profound and sustained blockade of thermal stimuli is produced in a dose-dependent fashion. Similar administration in dogs with bone cancer produces a prolonged antinociceptive response.
47
Sasaki, Tsutomu, Yoshihiro Kinoshita, Sho Matsui, Shigeru Kakuta, Hiromi Yokota-Hashimoto, Kuni Kinoshita, Yusaku Iwasaki, et al. "N-methyl-d-aspartate receptor coagonist d-serine suppresses intake of high-preference food." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 5 (September 2015): R561—R575. http://dx.doi.org/10.1152/ajpregu.00083.2015.
Full textAbstract:
d-Serine is abundant in the forebrain and physiologically important for modulating excitatory glutamatergic neurotransmission as a coagonist of synaptic N-methyl-d-aspartate (NMDA) receptor. NMDA signaling has been implicated in the control of food intake. However, the role of d-serine on appetite regulation is unknown. To clarify the effects of d-serine on appetite, we investigated the effect of oral d-serine ingestion on food intake in three different feeding paradigms (one-food access, two-food choice, and refeeding after 24-h fasting) using three different strains of male mice (C57Bl/6J, BKS, and ICR). The effect of d-serine was also tested in leptin signaling-deficient db/ db mice and sensory-deafferented (capsaicin-treated) mice. The expression of orexigenic neuropeptides [neuropeptide Y ( Npy) and agouti-related protein ( Agrp)] in the hypothalamus was compared in fast/refed experiments. Conditioned taste aversion for high-fat diet (HFD) was tested in the d-serine-treated mice. Under the one-food-access paradigm, some of the d-serine-treated mice showed starvation, but not when fed normal chow. HFD feeding with d-serine ingestion did not cause aversion. Under the two-food-choice paradigm, d-serine suppressed the intake of high-preference food but not normal chow. d-Serine also effectively suppressed HFD intake but not normal chow in db/ db mice and sensory-deafferented mice. In addition, d-serine suppressed normal chow intake after 24-h fasting despite higher orexigenic gene expression in the hypothalamus. d-Serine failed to suppress HFD intake in the presence of L-701,324, the selective and full antagonist at the glycine-binding site of the NMDA receptor. Therefore, d-serine suppresses the intake of high-preference food through coagonism toward NMDA receptors.
48
Bakpa, Emily Patience, Jianming Xie, Jing Zhang, Kangning Han, Yufeng Ma, and Tiandong Liu. "Influence of soil amendment of different concentrations of amino acid water-soluble fertilizer on physiological characteristics, yield and quality of “Hangjiao No.2” Chili Pepper." PeerJ 9 (November 29, 2021): e12472. http://dx.doi.org/10.7717/peerj.12472.
Full textAbstract:
Amino acids are well known as natural stimulators of plant growth and are widely used to promote crop yield and quality. Several studies have been conducted to investigate the effects of amino acid (s) as a foliar spray on a variety of plant species. However, the effects of soil amendment of different concentrations of amino acid water-soluble fertilizer on the physiological characteristics, yield, and quality of pepper remain unclear. Following this, three experimental sets of amino acid water-soluble fertilizer in the ratio 1.8: 2.7: 3.6 kg including control (CK) were conducted in Lintao county, Gansu province. The treatments were applied through furrow method at 6 weeks after planting. The results showed that physiological characteristics of the pepper plants, such as chlorophyll a (1.35 mg g−1), and b (0.67 mg g−1), total chlorophyll (2.02 mg g−1), carotenoid (0.63 mg g−1), ETR (26.25 µmol m−2s−1), Fv/Fm (0.75), Qp (0.92) contents of the leaves were increased by the 1.8 kg treatment while NPQ (71.37%) and root activity (2185.52 µg g−1 h−1) were improved by the 3.6 kg treatment compared to the control. Fertilization with 2.7 kg of amino acid water-soluble fertilizer also had a significant influence on fruit length (25.50 cm), and yield of pepper (37.92 t ha−1) while fruit diameter (24.51 mm), firmness (5.30 kg cm−2), fresh (48.10 g) and dry (4.71 g) weights were higher in the 1.8 kg treatment compared to the control. The lowest rate of fertilizer (1.8 kg) applied again resulted in a significant increase in soluble protein (79.79%), capsaicin (5.80 mg g−1), dihydrocapsaicin (1.08 mg g−1), vitamin C (72.33%) and the essential and non-essential amino acid contents of the pepper which ranged from (235.15 to 11.16 µg g−1) and (1,605.10 to 16.63 µg g−1) respectively, while soluble sugar (9.02%) was enhanced by 3.6 kg treatment compared to the control. The findings suggest that soil amendment with low concentration of amino acid water-soluble fertilizer (1.8 kg) could be successfully used to improve the physiological characteristics and fruit quality of peppers in vegetable production.
49
Rolls, Edmund T., Justus V. Verhagen, and Mikiko Kadohisa. "Representations of the Texture of Food in the Primate Orbitofrontal Cortex: Neurons Responding to Viscosity, Grittiness, and Capsaicin." Journal of Neurophysiology 90, no. 6 (December 2003): 3711–24. http://dx.doi.org/10.1152/jn.00515.2003.
Full textAbstract:
The primate orbitofrontal cortex (OFC) is a site of convergence from taste, olfactory, and somatosensory cortical areas. We describe a population of single neurons in the macaque OFC that responds to the texture of food in the mouth. Use of oral viscosity stimuli consisting of carboxymethylcellulose (CMC) in the range 1–10,000 centipoise showed that the responses of one subset of these neurons were related to stimulus viscosity. Some of the neurons had increasing responses to increasing viscosity, some had decreasing responses, and some neurons were tuned to a range of viscosities. These neurons are a different population to oral fat-sensitive neurons, in that their responses to fats (e.g., safflower oil), to silicone oil [(Si(CH3)2O)n], and to mineral oil (hydrocarbon) depended on the viscosity of these oils. Thus there is a dissociation between texture channels used to sense viscosity and fat. Some of these viscosity-sensitive single neurons were unimodal (somatosensory; 25%) and some received convergent taste inputs (75%). A second subpopulation of neurons responded to gritty texture (produced by microspheres suspended in CMC). A third subpopulation of neurons responded to capsaicin. These results provide evidence about the information channels used to represent the texture and flavor of food in a part of the brain important in appetitive responses to food and are relevant to understanding the physiological and pathophysiological processes related to food intake, food selection, and the effects of variety of food texture in combination with taste and other inputs that affect food intake.
50
Feuerstein, Glora, Robert Willette, and Nambi Aiyar. "Clinical perspectives of calcitonin gene related peptide pharmacology." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 1995): 1070–74. http://dx.doi.org/10.1139/y95-152.
Full textAbstract:
Calcitonin gene related peptide (CGRP), a potent vasoactive and cardiotonic peptide, interacts with specific G-protein-coupled receptors. CGRP is synthesized and released from small, capsaicin-sensitive sensory nerves. This extensive network of sensory nerves, found in virtually all organs, suggest a potential role for CGRP in diverse physiologic and pathophysiologic processes. The potent vasodilation elicited by CGRP in the cerebral, coronary, and peripheral vasculature has led to its therapeutic evaluation in the treatment of cerebral vasospasm following subarachnoid hemorrhage, stable angina, and Raynaud's phenomenon. The potential inotropic action and coronary vasodilation have also led to a potential beneficial effect in congestive heart failure. The enriched localization of CGRP in trigeminal sensory ganglia may indicate a role in the neurogenic inflammation associated with migraine. Thus, CGRP antagonists may represent a novel therapeutic approach to the treatment of migraine. In addition, CGRP and amylin (homologous pancreatic peptide) reduce the tissue–glucose response to insulin. It has been suggested that a CGRP antagonist may therefore improve insulin sensitivity in non-insulin-dependent diabetes, NIDDM. This brief review provides a preliminary exploration of the potential therapeutic opportunities surrounding CGRP and CGRP antagonists. Future advances are dependent on a better understanding of the structure and function of CGRP receptor(s) and the concomitant identification of selective and potent agonists and antagonists useful for addressing therapeutic hypotheses.Key words: calcitonin gene related peptide, congestive heart failure, diabetes, therapy, vasospasm, migraine.