Mechanism of vasorelaxant effect of the indole alkaloid 12-hydroxynorfluorocurarine hydrochloride on aortic smooth muscle contraction

This article examines the mechanism of action of 12-hydroxynorfluorocurarine hydrochloride on vascular contractile activity.The studies were conducted in vitro using rat aortic rings.The isometric force of the contractile force of the rings was measured using an FT-03 force transducer (Grass Instrument, USA).12-Hydroxynorfluorocurarine hydrochloride produced a dose-dependent vasorelaxant response on phenylephrine-induced aortic ring contractility, with the vasorelaxant response being reduced in the absence of endothelium.The vasorelaxant effect of 12-hydroxynorfluorocurarine hydrochloride is driven by modulation of the endothelial NO synthase (eNOS), guanylate cyclase (sGC), inward-rectifier K + channels (K ir ), and Ca 2+ -activated K + channels.Furthermore, when 50 mM KCl is present, this indole alkaloid was observed to diminish the force of aortic contraction induced by elevated Ca² + ion concentration.12-Hydroxynorfluorocurarine hydrochloride has been shown to exert potent vasorelaxant effects on rat aortic preparations through both endothelium-dependent and endothelium-independent pathways.It has been shown that the vasorelaxant action of 12-hydroxynorfluorocurarine hydrochloride is mediated by blocking L-type Ca 2+ channels via the eNOS/NO/sGC signaling cascade and by activating K ir channels.