Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat

Purpose Angiotensin II (Ang II)-induced vasoconstriction is mediated by changes in intracellular free Ca 2+ concentration ([Ca 2+ ] i ) and myofilament Ca 2+ sensitivity. Protein kinase C- and Rho kinase-mediated signaling pathways are proposed for the regulation of the Ca 2+ sensitization mechanisms. We have demonstrated that sevoflurane inhibits Rho kinase-mediated contraction of isolated rat aortic smooth muscle. A recent study demonstrated that Rho-kinase mediated Ca 2+ sensitization was involved in the pathophysiology of hypertension. This study was designed to investigate the effects of sevoflurane on Ang II-induced Rho kinase-mediated vascular contraction in spontaneously hypertensive rats (SHR). Methods The effects of sevoflurane on vasoconstriction, increase in [Ca 2+ ] i , and membrane translocation of Rho kinase in response to Ang II were investigated in normotensive Wistar–Kyoto rats (WKY) and SHR, using an isometric force transducer, a fluorometer, and Western blotting, respectively. Results The inhibitory effects of sevoflurane on Ang II (10 −7 M)-induced contraction were greater ( P