Augmentation of capsaicin-induced vasorelaxation of superior mesenteric artery (<i>Capra hircus</i>) in acidosis: role of TRPV1 channels

Abstract

Capsaicin is known to induce vasorelaxation through activation of the transient receptor potential cation channel subfamily V member 1(TRPV1). However, TRPV1 is a nonselective cation channel and can be activated by a wide variety of exogenous and endogenous stimuli, including acidic conditions. The present study investigated the effect of changes in <i>p</i>H on capsaicin-induced vasorelaxation in both endothelium intact and denuded goat superior mesenteric artery (GSMA) rings, using a highly sensitive isometric force transducer. There was a significant increase in capsaicin-induced vasorelaxation in nor adrenaline (NA)-precontracted GSMA rings at acidic <i>p</i>Hs of 6.8 (44.71±4.85%) and <i>p</i>H 6.0 (46.43±2.59%), compared to a physiological level of <i>p</i>H of 7.4 (33.25±2.62%). Although not completely abrogated, endothelium denudation and ruthenium red (RR) treatment significantly attenuated capsaicin-induced vasorelaxation at all <i>p</i>H levels. These data together suggest that, while other minor endothelium/TRVP1-independent mechanisms may exist, augmentation of capsaicin-induced vasorelaxation in acidosis is primarily endothelium-dependent and mediated through TRPV1 channels.