Halothane attenuates the endothelial Ca2+ increase and vasorelaxation of vascular smooth muscle in the rat aorta

Abstract

Isolated spiral strips of rat thoracic aorta with endothelium were suspended for isometric tension recordings in a physiological salt solution. Endothelium-dependent vasorelaxation was elicited by carbachol 10-6 and 10-5 mol litre-1 during norepinephrine-induced contractions, and the effects of 1.5% and 3% halothane were evaluated with concomitant measurement of [Ca2+](i) using fura-2-Ca2+ fluorescence. The effects of halothane on endothelium-dependent relaxation were compared with those of nitro(G)-L-arginine methyl ester 10-4 mol litre-1 (L-NAME: an inhibitor of nitric oxide synthase). Carbachol reduced norepinephrine-induced contractions in a concentration-dependent manner, but augmented the norepinephrine-induced increase in [Ca2+](i) in endothelium intact strips. In contrast, carbachol did not influence muscle tension or [Ca2+](i) when the endothelium was completely denuded. Although 3% halothane and L-NAME 10-4 mol litre-1 inhibited carbachol-induced vasorelaxation in a similar manner, halothane inhibited carbachol-induced increases in [Ca2+](i). These results indicate that halothane inhibited a carbachol-induced increase in [Ca2+](i) in the endothelium, which subsequently attenuated the decrease in muscle tension.