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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 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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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
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ISSN: | 0913-8668 1438-8359 |
DOI: | 10.1007/s00540-011-1121-8 |