Participation of the TRP channel in the cardiovascular effects induced by carvacrol in normotensive rat.

Abstract Carvacrol has been described as an agonist/antagonist of different transient receptor potential (TRP) channels and voltage-dependent calcium channels (Ca v s). The aim of this study was to evaluate the role of Ca v and TRP channels following carvacrol stimulation. Initially, in mesenteric artery rings carvacrol relaxed phenylephrine-induced contractions. Furthermore, carvacrol inhibited contraction elicited by CaCl 2 in depolarizing nominally without Ca 2 + medium and antagonized the contractions induced by S(−)-Bay K 8644 and inhibited Ca 2 + currents indicating the inhibition of Ca 2 + influx through L-type Ca v . Additionally, carvacrol antagonized the contractions induced by CaCl 2 in the presence of nifedipine/Cyclopiazonic acid/phenylephrine or nifedipine/Cyclopiazonic acid/KCl 60, suggesting a possible inhibition of calcium influx by store operated channels (SOCs), receptor operated channels (ROCs) and/or TRP channels. Interestingly, among the TRP channel blockers used, the effect induced by carvacrol was attenuated by Mg 2 + and potentiated by La 3 + and Gd 3 + , suggesting that TRP channels are involved in relaxation induced by carvacrol. Monoterpene also induced hypotension and bradycardia in non-anesthetized normotensive rats and negative inotropic and chronotropic effects. In conclusion, these results suggest that the hypotensive effect of carvacrol is probably due to bradycardia and a peripheral vasodilatation that involves, at least, the inhibition of the Ca 2 + influx through Ca v and TRP channels.