scholarly journals Protective Effects of TRPV1 Activation Against Cardiac Ischemia/ Reperfusion Injury is Blunted by Diet-Induced Obesity

2020 ◽  
Vol 20 (2) ◽  
pp. 122-130
Author(s):  
Beihua Zhong ◽  
Shuangtao Ma ◽  
Donna H. Wang
Keyword(s):  
Infarct Size ◽  
Transient Receptor Potential ◽  
Diastolic Pressure ◽  
Gene Knockout ◽  
Ischemia Reperfusion ◽  
Control Diet ◽  
Left Ventricular ◽  
Transient Receptor Potential Vanilloid ◽  
Trpv1 Channels ◽  
Postischemic Recovery

Background: Activation of Transient Receptor Potential Vanilloid Subtype 1 (TRPV1) channels protects the heart from Ischemia/Reperfusion (I/R) injury through releasing Calcitonin Gene-Related Peptide (CGRP) and Substance P (SP). The current study aimed to study the cardioprotective effects of TRPV1 in obesity. Methods: TRPV1 gene knockout (TRPV1-/-) and Wild-Type (WT) mice were Fed a High-Fat Diet (HFD) or a control diet or for 20 weeks, and then the hearts were collected for I/R injury ex vivo. The hearts were mounted on a Langendorff apparatus and subjected to ischemia (30 min) and reperfusion (40 min) after incubated with capsaicin (10 nmol/L), CGRP (0.1 μmol/L) and SP (0.1 μmol/L). Then, Coronary Flow (CF), left ventricular peak positive dP/dt (+dP/dt), Left Ventricular Developed Pressure (LVDP) and Left Ventricular End-Diastolic Pressure (LVEDP) were measured. Results: HFD intake remarkably reduced CF, +dP/dt and LVDP and elevated LVEDP in both strains (P<0.05). Treatment with capsaicin decreased infarct size, increased CF, +dP/dt and LVDP, and decreased LVEDP in WT mice on control diet (P<0.05), but did not do so in other three groups. Treatment with CGRP and SP decreased infarct size in both strains fed with control diet (P<0.05). In contrast, not all the parameters of cardiac postischemic recovery in HFD-fed WT and TRPV1-/- mice were improved by CGRP and SP. Conclusions: These results suggest that HFD intake impairs cardiac postischemic recovery. HFDinduced impairment of recovery is alleviated by CGRP in both strains and by SP only in TRPV1-/- mice, indicating that the effects of CGRP and SP are differentially regulated during HFD intake.

TRPV1 gene knockout impairs preconditioning protection against myocardial injury in isolated perfused hearts in mice

2007 ◽  
Vol 293 (3) ◽  
pp. H1791-H1798 ◽  
Author(s):  
Beihua Zhong ◽  
Donna H. Wang
Keyword(s):  
Substance P ◽  
Receptor Antagonist ◽  
Transient Receptor Potential ◽  
Diastolic Pressure ◽  
Gene Knockout ◽  
Receptor Potential ◽  
Nerve Fibers ◽  
Left Ventricular ◽  
Transient Receptor Potential Vanilloid ◽  
Beneficial Effects

Although the transient receptor potential vanilloid type 1 (TRPV1)-containing afferent nerve fibers are widely distributed in the heart, the relationship between TRPV1 function and cardiac ischemic preconditioning (PC) has not been well defined. Using TRPV1 knockout mice (TRPV1−/−), we studied the role of TRPV1 in PC-induced myocardial protection. Hearts of gene-targeted TRPV1-null mutant (TRPV1−/−) or wild-type (WT) mice were Langendorffly perfused in the presence or absence of CGRP8-37, a selective calcitonin gene-related peptide (CGRP) receptor antagonist; or RP-67580, a selective neurokinin-1 receptor antagonist when hearts were subjected to three 5-min periods of ischemia PC followed by 30 min of global ischemia and 40 min of reperfusion (I/R). PC before I/R decreased left ventricular (LV) end-diastolic pressure and increased LV developed pressure, coronary flow (CF), peak-positive maximum rate of rise of LV pressure in WT mice (PC-WT) compared with PC-TRPV1−/−, TRPV1−/−, or WT hearts ( P < 0.05), and PC also decreased LV end-diastolic pressure in PC-TRPV1−/− compared with TRPV1−/−. CGRP8-37 or RP-67580 abolished PC-induced protection in WT but not TRPV1−/− hearts ( P < 0.05). Moreover, PC decreased lactate dehydrogenase release and infarct size in PC-WT compared with PC-TRPV1−/−, TRPV1−/−, or WT hearts, and it also lowered these parameters in PC-TRPV1−/− compared with TRPV1−/− hearts ( P < 0.05). Radioimmunoassay showed that the release of substance P and CGRP after PC was higher in WT hearts than in TRPV1−/− hearts ( P < 0.05), which was attenuated by capsazepine in WT but not TRPV1−/− hearts. Thus PC-induced protection of the heart was impaired in TRPV1−/− hearts, indicating that TRPV1 contributes to the beneficial effects of preconditioning against I/R injury through release substance P and CGRP.

scholarly journals N-oleoyldopamine, a novel endogenous capsaicin-like lipid, protects the heart against ischemia-reperfusion injury via activation of TRPV1

2008 ◽  
Vol 295 (2) ◽  
pp. H728-H735 ◽  
Author(s):  
Beihua Zhong ◽  
Donna H. Wang
Keyword(s):  
Protective Effect ◽  
Receptor Antagonist ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion Injury ◽  
Diastolic Pressure ◽  
Ischemia Reperfusion ◽  
Receptor Potential ◽  
Left Ventricular ◽  
Mammalian Brain ◽  
Transient Receptor Potential Vanilloid

N-oleoyldopamine (OLDA), a bioactive lipid originally found in the mammalian brain, is an endovanilloid that selectively activates the transient receptor potential vanilloid type 1 (TRPV1) channel. This study tests the hypothesis that OLDA protects the heart against ischemia and reperfusion (I/R) injury via activation of the TRPV1 in wild-type (WT) but not in gene-targeted TRPV1-null mutant (TRPV1−/−) mice. Hearts of WT or TRPV1−/− mice were Langendorffly perfused with OLDA (2 × 10−9 M) in the presence or absence of CGRP8–37 (1 × 10−6 M), a selective calcitonin gene-related peptide (CGRP) receptor antagonist; RP-67580 (1 × 10−6 M), a selective neurokinin-1 receptor antagonist; chelerythrine (5 × 10−6 M), a selective protein kinase C (PKC) antagonist; or tetrabutylammonium (TBA, 5 × 10−4 M), a nonselective K+ channel antagonist, followed by 35 min of global ischemia and 40 min of reperfusion (I/R). Left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), coronary flow (CF), and left ventricular peak positive dP/d t (+dP/d t) were evaluated after I/R. OLDA improved recovery of cardiac function after I/R in WT but not TRPV1−/− hearts by increasing LVDP, CF, and +dP/d t and by decreasing LVEDP. CGRP8–37, RP-67580, chelerythrine, or TBA abolished the protective effect of OLDA in WT hearts. Radioimmunoassay showed that the release of substance P (SP) and CGRP after OLDA treatment was higher in WT than in TRPV1−/− hearts, which was blocked by chelerythrine or TBA. Thus OLDA exerts a cardiac protective effect during I/R injury in WT hearts via CGRP and SP release, which is abolished by PKC or K+ channel antagonists. The protective effect of OLDA is void in TRPV1−/− hearts, supporting the notion that TRPV1 mediates OLDA-induced protection against cardiac I/R injury.

scholarly journals Protease-activated receptor 2-mediated protection of myocardial ischemia-reperfusion injury: role of transient receptor potential vanilloid receptors

2009 ◽  
Vol 297 (6) ◽  
pp. R1681-R1690 ◽  
Author(s):  
Beihua Zhong ◽  
Donna H. Wang
Keyword(s):  
Transient Receptor Potential ◽  
Diastolic Pressure ◽  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Receptor Potential ◽  
Left Ventricular ◽  
Transient Receptor Potential Vanilloid ◽  
Transient Receptor ◽  
Myocardial Ischemia Reperfusion ◽  
Developed Pressure

Activation of the protease-activated receptor 2 (PAR2) or the transient receptor potential vanilloid type 1 (TRPV1) channels expressed in cardiac sensory afferents containing calcitonin gene-related peptide (CGRP) and/or substance P (SP) has been proposed to play a protective role in myocardial ischemia-reperfusion (I/R) injury. However, the interaction between PAR2 and TRPV1 is largely unknown. Using gene-targeted TRPV1-null mutant (TRPV1−/−) or wild-type (WT) mice, we test the hypothesis that TRPV1 contributes to PAR2-mediated cardiac protection via increasing the release of CGRP and SP. Immunofluorescence labeling showed that TRPV1 coexpressed with PAR2, PKC-ε, or PKAc in cardiomyocytes, cardiac blood vessels, and perivascular nerves in WT but not TRPV1−/− hearts. WT or TRPV1−/− hearts were Langendorff perfused with the selective PAR2 agonist, SLIGRL, in the presence or absence of various antagonists, followed by 35 min of global ischemia and 40 min of reperfusion (I/R). The recovery rate of coronary flow, the maximum rate of left ventricular pressure development, left ventricular end-diastolic pressure, and left ventricular developed pressure were evaluated after I/R. SLIGRL improved the recovery of hemodynamic parameters, decreased lactate dehydrogenase release, and reduced the infarct size in both WT and TRPV1−/− hearts ( P < 0.05). The protection of SLIGRL was significantly surpassed for WT compared with TRPV1−/− hearts ( P < 0.05). CGRP8–37, a selective CGRP receptor antagonist, RP67580, a selective neurokinin-1 receptor antagonist, PKC-ε V1–2, a selective PKC-ε inhibitor, or H-89, a selective PKA inhibitor, abolished SLIGRL protection by inhibiting the recovery of the rate of coronary flow, maximum rate of left ventricular pressure development, and left ventricular developed pressure, and increasing left ventricular end-diastolic pressure in WT but not TRPV1−/− hearts. Radioimmunoassay showed that SLIGRL increased the release of CGRP and SP in WT but not TRPV1−/− hearts ( P < 0.05), which were prevented by PKC-ε V1–2 and H-89. Thus our data show that PAR2 activation improves cardiac recovery after I/R injury in WT and TRPV1−/− hearts, with a greater effect in the former, suggesting that PAR2-mediated protection is TRPV1 dependent and independent, and that dysfunctional TRPV1 impairs PAR2 action. PAR2 activation of the PKC-ε or PKA pathway stimulates or sensitizes TRPV1 in WT hearts, leading to the release of CGRP and SP that contribute, at least in part, to PAR2-induced cardiac protection against I/R injury.

Abstract 54: Probenecid Improves Myocardial Function in an Ischemic Heart Disease Murine Model

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Nathan Robbins ◽  
Sheryl E Koch ◽  
Min Jiang ◽  
Michael Tranter ◽  
Xiaoping Ren ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Infarct Size ◽  
Cell Viability ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Heart ◽  
Transient Receptor Potential Vanilloid ◽  
High Concentrations

Introduction Probenecid, previously used for the treatment of gout, is a transient receptor potential vanilloid 2 (TRPV2) agonist. We have found TRPV2 in murine cardiomyocytes and when stimulated by probenecid, results in a positive inotropic response through Ca 2+ influx independent of β-adrenergic signaling. Our hypothesis is that probenecid will increase contractility without affecting cell survival. Methods We studied the role of probenecid as a positive inotrope in a mouse model of ischemic heart disease. We administered probenecid via intraperitoneal injections (100mg/kg) before and after ischemia/reperfusion injury (I/R) and orally via treated water (100mg/kg daily for 4 weeks), using saline injections and untreated water as respective controls. Ischemia was induced by a 45 minute ligation of the LAD followed by reperfusion and all mice were followed serially via echocardiography. We also evaluated the effects of probenecid on HL-1 cell apoptosis by conducting cell viability assays. Results Treatment with probenecid before I/R had no effect on subsequent infarct size (51.6±3.71% vs. 53.4±1.54%;P=NS). However, post-I/R probenecid caused an increase in ejection fraction (EF) of 10.9±1.98% in mice with initial EF between 40-50% (n=6; P<0.01) and 7.28±1.63% in mice with higher initial EF (50-60%) (n=6; p<0.01). Echocardiographic analysis of mice with oral probenecid after I/R demonstrated higher EF and smaller diastolic volume (47.19±2.29%; 79.57mL±1.63; n=6) compared to untreated mice (43.67±2.91%; 89.05mL±5.67; n=6). Cell viability assays showed high concentrations of probenecid had minimal effect on cell viability (88.6±6.2% of control) whereas treatment with high concentrations of isoproterenol (10mM) greatly decreased cell viability (6.7±0.1% of control). Conclusions These experiments demonstrate 1) probenecid increases myocardial contractility at baseline and significantly more so after I/R injury; 2) probenecid therapy improves function when used chronically; 3) the increase in contractility is not associated with either increased infarct size in vivo or apoptosis in vitro. Thus, unlike other positive inotropes, such as isoproterenol, probenecid increases contractility without resulting in significant cell death.

Abstract 17443: Inhibition of the Calcineurin Interaction Site on TRPV1 Reduces Myocardial Infarct Size in Rats

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Eric R Gross ◽  
Nir Qvit ◽  
Garrett J Gross ◽  
Daria Mochly-Rosen
Keyword(s):  
Infarct Size ◽  
Transient Receptor Potential ◽  
Myocardial Infarct ◽  
Ischemia Reperfusion ◽  
In Vivo Studies ◽  
Transient Receptor Potential Vanilloid ◽  
Myocardial Infarct Size ◽  
Interaction Site ◽  
Calcineurin Activity

Introduction: With recent public concerns of opioid overuse, misuse and addiction along with the heightened FDA restrictions on opioid prescribing, non-opioid cardiac-safe pain therapeutics for those with cardiovascular disease is needed. The transient receptor potential vanilloid 1 (TRPV1), a mediator of heat, pain and noxious stimuli, mediates nociception. While blocking TRPV1 reduces pain, the finding preconditioning-induced cardioprotection is lost in TRPV1 knockout mice or by TRPV1 inhibition indicates a dual role for TRPV1 both in protection from cardiac injury and in pain signaling. Hypothesis: We tested whether a peptide corresponding to a calcineurin interaction site on TRPV1 could separate the functions of TRPV1 by reducing myocardial injury while providing pain control. Methods: The peptide was synthesized using a Liberty peptide synthesizer and conjugated to TAT for intracellular entry. Male Sprague-Dawley rats 8 weeks of age were used for both isolated heart and in vivo studies consisting of 30 minutes of ischemia followed by reperfusion. Infarct size was assessed by triphenyltetrazolium staining. Results: Testing the peptide using a calcineurin activity assay kit in vitro showed the peptide inhibited calcineurin activity vs. TAT control (0.46±0.03* vs. 0.77±0.02, nmol phosphate, n=3/group, *P<0.05). Further, peptide treatment of isolated hearts (1μM, infused over 10 minutes prior to ischemia) reduced infarct size and creatine phosphokinase (CPK) release when compared to TAT-treated hearts (Infarct size: 19±3%* vs. 53±4%, %infarct/left ventricle; CPK: 69±22* vs. 459±132, n=6/group, *P<0.01). In an in vivo myocardial ischemia-reperfusion model, the peptide (1mg/kg), given subcutaneously to the abdominal skin prior to ischemia, reduced infarct size compared to control (50±2*% vs. 66±1%, *P<0.001). Initial evidence also suggests that the peptide provides analgesia in pain models. Conclusions: Our results suggest a peptide blocking the calcineurin interaction site of TRPV1 reduces myocardial infarct size. Therefore, disrupting specific protein-protein interactions between calcineurin and TRPV1 may provide a novel strategy to design non-opioid therapeutics for cardioprotection, while also providing pain relief.

Simulated microgravity increases myocardial susceptibility to ischemia–reperfusion injury via a deficiency of AMP-activated protein kinase

2017 ◽  
Vol 95 (1) ◽  
pp. 59-71 ◽  
Author(s):  
Yuan-Ming Lu ◽  
Bo Jiao ◽  
Jun Lee ◽  
Lin Zhang ◽  
Zhi-Bin Yu
Keyword(s):  
Protein Kinase ◽  
Infarct Size ◽  
Simulated Microgravity ◽  
Ischemia Reperfusion Injury ◽  
Diastolic Pressure ◽  
Ischemia Reperfusion ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ampk Phosphorylation ◽  
Amp Activated Protein Kinase

Gravitation is an important factor in maintaining cardiac contractility. Our study investigated whether simulated microgravity increases myocardial susceptibility to ischemia–reperfusion (IR) injury. Using the Langendorff-perfused heart model with 300 beats/min pacing, 4-week tail suspension (SUS) and control (CON) male Sprague-Dawley rats (n = 10 rats/group) were subjected to 60 min of left anterior descending coronary artery (LAD) occlusion followed by 120 min of reperfusion. Left ventricular end-systolic pressure (LVESP), left ventricular end-diastolic pressure (LVEDP), creatine kinase (CK) and lactate dehydrogenase (LDH) activity, and infarct size were assessed. Data demonstrated that there were significantly increased LVEDP, CK, LDH, and infarct size in SUS compared with CON (P < 0.05), accompanied by decreased LVESP (P < 0.05). Furthermore, TUNEL-positive cardiomyocytes were higher in SUS than that in CON (P < 0.01), and AMP-activated protein kinase (AMPK) phosphorylation and Bcl-2/Bax in SUS were less compared with CON (P < 0.05). Similarly, isolated hearts pre-treated with A-769662 exhibited better recovery of cardiac function, increased AMPK phosphorylation, and reduced necrosis and apoptosis. Furthermore, AMPKα protein showed a significant suppression in 4-week hindlimb unweighting rats. These results suggest that AMPK deficiency increases myocardial susceptibility to IR injury in rats subjected to simulated microgravity.

A Review on Potential Involvement of TRPV1 Channels in Ischemia–Reperfusion Injury

2017 ◽  
Vol 23 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Puneet Kaur Randhawa ◽  
Amteshwar Singh Jaggi
Keyword(s):  
Reperfusion Injury ◽  
Inflammatory Cytokines ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Channel Activation ◽  
Trpv1 Channels ◽  
Transient Receptor

Besides functioning as thermosensors, transient receptor potential vanilloid 1 (TRPV1) channels play a pivotal role in ischemia–reperfusion injury. Transient receptor potential vanilloid 1 channel activation attenuates ischemia–reperfusion-induced injury in various organs including the heart, lungs, kidneys, and the brain. Transient receptor potential vanilloid 1 channels are expressed on the sensory neurons innervating the myocardium, ventricles of the heart, epicardial surface of the heart, endothelial cells, and the vascular smooth muscle cells. During ischemic conditions, activation of TRPV1 channels on the perivascular nerves stimulates the release of calcitonin gene-related peptide and substance P to produce cardioprotection. Furthermore, TRPV1 channel activation reduces the generation of free radicals and inflammatory cytokines, inhibits neutrophil infiltration, and enhances the production of anti-inflammatory cytokines to reduce ischemia–reperfusion-induced tissue injury. The present review describes the potential involvement of TRPV1 channels and the signaling cascade in attenuating ischemia–reperfusion injury in various organs.

Na+/H+ exchange inhibition attenuates hypertrophy and heart failure in 1-wk postinfarction rat myocardium

2000 ◽  
Vol 278 (1) ◽  
pp. H300-H304 ◽  
Author(s):  
Hiroyuki Yoshida ◽  
Morris Karmazyn
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Diastolic Pressure ◽  
Ph Regulation ◽  
Control Diet ◽  
Left Ventricular ◽  
Heart Weight ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
Drug Concentrations

Na+/H+ exchange (NHE) represents a major mechanism for intracellular pH regulation, particularly in the ischemic myocardium. NHE has also been shown to be important in the regulation of cell proliferation and growth. We examined whether inhibition of NHE results in an attenuation of early postinfarction myocyte remodeling responses in the rat. Male Sprague-Dawley rats were randomized to receive either a control diet or an identical diet supplemented with the NHE inhibitor cariporide. After 1 wk, animals were anesthetized, subjected to ligation of the left main coronary artery, and maintained for an additional week, after which time they were anesthetized and intraventricular pressures were obtained. Hearts were removed, and myocytes were isolated to obtain cell dimensions and determine the response to isoproterenol. Body, heart, and lung weights were obtained. Coronary artery ligation in control animals resulted in a significant elevation in left ventricular end-diastolic pressure, as well as increased heart weight- and lung weight-to-body weight ratios, both of which were abrogated by cariporide. Cell length and area significantly increased by 14 and 19.2%, respectively, whereas cell width increased by 4.1% ( P> 0.05). These cells exhibited a significant hyporesponsiveness to the positive inotropic responses to isoproterenol at the lower drug concentrations (3 and 10 nM). A <1% dimensional change occurred in myocytes from cariporide-fed animals, and the hyporesponse to isoproterenol was reversed. Cariporide had no effect on infarct size or blood pressure. These studies suggest that the early adaptive hypertrophic response of surviving myocytes is dependent on NHE activity. As such, it is attractive to suggest that NHE inhibition could be an effective therapeutic strategy for prevention of postinfarction remodeling, independent of infarct size or afterload reduction.

scholarly journals Cardioprotective effect of fingolimod against calcium paradox-induced myocardial injury in the isolated rat heart

2021 ◽  
Author(s):  
Fatma Alatrag ◽  
Matthew Amoni ◽  
Roisin Kelly-Laubscher ◽  
Asfree Gwanyanya
Keyword(s):  
Infarct Size ◽  
Transient Receptor Potential ◽  
Diastolic Pressure ◽  
Myocardial Infarct ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Myocardial Infarct Size ◽  
Hemodynamic Parameters ◽  
Transient Receptor Potential Melastatin ◽  
Ventricular Tissue

Fingolimod (FTY720) inhibits Ca<sup>2+</sup>-permeable, Mg<sup>2+</sup>-sensitive channels called transient receptor potential melastatin 7 (TRPM7), but its effects on Ca<sup>2+</sup> paradox (CP)-induced myocardial damage have not been evaluated. We studied the effect of FTY720 on CP-induced myocardial damage, and used other TRPM7 channel inhibitors nordihydroguaiaretic acid (NDGA) and Mg<sup>2+</sup> to test if any effect of FTY720 was via TRPM7 inhibition. Langendorff-perfused Wistar rat hearts were treated with FTY720 or NDGA and subjected to a CP protocol consisting of Ca<sup>2+</sup> depletion followed by Ca<sup>2+</sup> repletion. Hearts of rats pre-treated with MgSO<sub>4</sub> were also subjected to CP. Hemodynamic parameters were measured using an intraventricular balloon, and myocardial infarct size was quantified using triphenyltetrazolium chloride stain. TRPM7 proteins in ventricular tissue were detected using immunoblot analysis. FTY720, but not NDGA, decreased CP-induced infarct size. Both FTY720 and NDGA minimized the CP-induced elevation of left ventricular end-diastolic pressure, but only FTY720 ultimately improved ventricular developed pressure. Mg<sup>2+</sup> pre-treatment had effect neither on CP-induced infarct size, hemodynamic parameters during CP, nor the level TRPM7 protein expression in ventricular tissue. Overall, FTY720 attenuated CP-induced myocardial damage, with potential therapeutic implications on Ca<sup>2+</sup>-mediated cardiotoxicity. However, the cardioprotective mechanism of FTY720 seems to be unrelated to TRPM7 channel modulation.

scholarly journals Interactions between Chemesthesis and Taste: Role of TRPA1 and TRPV1

2021 ◽  
Vol 22 (7) ◽  
pp. 3360
Author(s):  
Mee-Ra Rhyu ◽  
Yiseul Kim ◽  
Vijay Lyall
Keyword(s):  
Transient Receptor Potential ◽  
Taste Receptor ◽  
Sensory Nerve ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Trpv1 Channels ◽  
Trigeminal Neurons ◽  
Calcitonin Gene ◽  
Transient Receptor

In addition to the sense of taste and olfaction, chemesthesis, the sensation of irritation, pungency, cooling, warmth, or burning elicited by spices and herbs, plays a central role in food consumption. Many plant-derived molecules demonstrate their chemesthetic properties via the opening of transient receptor potential ankyrin 1 (TRPA1) and transient receptor potential vanilloid 1 (TRPV1) channels. TRPA1 and TRPV1 are structurally related thermosensitive cation channels and are often co-expressed in sensory nerve endings. TRPA1 and TRPV1 can also indirectly influence some, but not all, primary taste qualities via the release of substance P and calcitonin gene-related peptide (CGRP) from trigeminal neurons and their subsequent effects on CGRP receptor expressed in Type III taste receptor cells. Here, we will review the effect of some chemesthetic agonists of TRPA1 and TRPV1 and their influence on bitter, sour, and salt taste qualities.

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