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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 mechanism...

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Published in:Journal of anesthesia 2011-06, Vol.25 (3), p.398-404
Main Authors: Uematsu, Nobuhiko, Ogawa, Koji, Tokinaga, Yasuyuki, Tange, Kazuaki, Hatano, Yoshio
Format: Article
Language:English
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Summary: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  
ISSN:0913-8668
1438-8359
DOI:10.1007/s00540-011-1121-8