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   <subfield code="a">10.1007/s00540-011-1121-8</subfield>
   <subfield code="2">doi</subfield>
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   <subfield code="a">(NATIONALLICENCE)springer-10.1007/s00540-011-1121-8</subfield>
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  <datafield tag="245" ind1="0" ind2="0">
   <subfield code="a">Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Nobuhiko Uematsu, Koji Ogawa, Yasuyuki Tokinaga, Kazuaki Tange, Yoshio Hatano]</subfield>
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   <subfield code="a">Purpose: Angiotensin II (Ang II)-induced vasoconstriction is mediated by changes in intracellular free Ca2+ concentration ([Ca2+] i ) and myofilament Ca2+ sensitivity. Protein kinase C- and Rho kinase-mediated signaling pathways are proposed for the regulation of the Ca2+ 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 Ca2+ 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 [Ca2+] 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 (10−7M)-induced contraction were greater (P&lt;0.05) in SHR than in WKY at the highest concentration of sevoflurane (5.1%). Y27632 (3×10−7M), a specific inhibitor of Rho kinase, inhibited the Ang II-induced contraction in SHR, but not in WKY. Sevoflurane did not affect the increases in [Ca2+] i in response to Ang II in either strain. Ang II stimulated Rho kinase activity in SHR, which was almost abolished by sevoflurane at a concentration of 5.1% (P&lt;0.05). Conclusions: These findings suggest that the inhibition of the Ang II-induced contraction by sevoflurane in SHR may be, at least in part, due to the attenuation of the Rho kinase-mediated signaling pathway.</subfield>
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   <subfield code="a">Japanese Society of Anesthesiologists, 2011</subfield>
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   <subfield code="a">Sevoflurane</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Hypertension</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Artery</subfield>
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   <subfield code="a">Rho kinase</subfield>
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   <subfield code="a">Uematsu</subfield>
   <subfield code="D">Nobuhiko</subfield>
   <subfield code="u">Department of Anesthesia, Japan Red Cross Society Wakayama Medical Center, Wakayama, Japan</subfield>
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   <subfield code="a">Ogawa</subfield>
   <subfield code="D">Koji</subfield>
   <subfield code="u">Department of Anesthesiology, Wakayama Medical University, 811-1 Kimiidera, 641-0012, Wakayama, Japan</subfield>
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   <subfield code="a">Tokinaga</subfield>
   <subfield code="D">Yasuyuki</subfield>
   <subfield code="u">Department of Anesthesiology, Wakayama Medical University, 811-1 Kimiidera, 641-0012, Wakayama, Japan</subfield>
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   <subfield code="a">Tange</subfield>
   <subfield code="D">Kazuaki</subfield>
   <subfield code="u">Department of Anesthesiology, Wakayama Medical University, 811-1 Kimiidera, 641-0012, Wakayama, Japan</subfield>
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   <subfield code="a">Hatano</subfield>
   <subfield code="D">Yoshio</subfield>
   <subfield code="u">Department of Anesthesiology, Wakayama Medical University, 811-1 Kimiidera, 641-0012, Wakayama, Japan</subfield>
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   <subfield code="t">Journal of Anesthesia</subfield>
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   <subfield code="g">25/3(2011-06-01), 398-404</subfield>
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