Carvacrol has been described as an agonist/antagonist of different transient receptor potential (TRP) channels and voltage-dependent calcium channels (Cavs). The aim of this study was to evaluate the role of Cav and TRP channels following carvacrol stimulation. Initially, in mesenteric artery rings carvacrol relaxed phenylephrine-induced contractions. Furthermore, carvacrol inhibited contraction elicited by CaCl2 in depolarizing nominally without Ca2+ medium and antagonized the contractions induced by S(-)-Bay K 8644 and inhibited Ca2+ currents indicating the inhibition of Ca2+ influx through L-type Cav. Additionally, carvacrol antagonized the contractions induced by CaCl2 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 Mg2+ and potentiated by La3+ and Gd3+, 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 Ca2+ influx through Cav and TRP channels.
Keywords: Carvacrol; L-type voltage-operated Ca(2+) channels; Rat superior mesenteric arterial; Transient receptor potential (TRP) channel; Vasorelaxant.
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