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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 |
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| cites | cdi_FETCH-LOGICAL-c567t-8a434c4fa6f76cbba3b502c77b65038e0794e34b143da0b68420a1aedcafd2ca3 |
| container_end_page | 404 |
| container_issue | 3 |
| container_start_page | 398 |
| container_title | Journal of anesthesia |
| container_volume | 25 |
| creator | Uematsu, Nobuhiko Ogawa, Koji Tokinaga, Yasuyuki Tange, Kazuaki Hatano, Yoshio |
| description | 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
|
| doi_str_mv | 10.1007/s00540-011-1121-8 |
| format | article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_871386202</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A356142123</galeid><sourcerecordid>A356142123</sourcerecordid><originalsourceid>FETCH-LOGICAL-c567t-8a434c4fa6f76cbba3b502c77b65038e0794e34b143da0b68420a1aedcafd2ca3</originalsourceid><addsrcrecordid>eNp9kk2LFDEQhoMo7rj6A7xIwIOnrPnqdOa4LOoOLAh-nEM6XZnJ2p2MSffA_IT912bsVRAGySFQed6qVNWL0GtGrxil7ftCaSMpoYwRxjgj-glaMSk00aJZP0UrumaCaKX0BXpRyj2lVDEmnqMLziRdi4at0MNXOCQ_zNlGwCHuQhemgm3chjRBLCHizYaE2M8Oevxll_CPEG0BMkIf7FRjLsUpWzeFFHHy-GCLmwebcRlTmnZ4nIsbAPucRlz2la110lyGI94d95B_1zgAznZ6iZ55OxR49Xhfou8fP3y7uSV3nz9tbq7viGtUOxFtpZBOeqt8q1zXWdE1lLu27VRDhQbariUI2dU59JZ2SktOLbPQO-t77qy4RO-WvPucfs5QJjOG4mAYlp8Z3TKhFae8km8XcmsHMCH6dOr0RJtr0SgmOeOiUuQMtYUI2Q4pgg81_A9_dYavp4cxuLMCtghcTqVk8Gafw2jz0TBqTj4wiw9M9YE5-cDoqnnz2OTc1VX9VfxZfAX4ApT6FLeQzX2ac6yD_0_WX-TIv5Y</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>871386202</pqid></control><display><type>article</type><title>Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat</title><source>Springer Link</source><creator>Uematsu, Nobuhiko ; Ogawa, Koji ; Tokinaga, Yasuyuki ; Tange, Kazuaki ; Hatano, Yoshio</creator><creatorcontrib>Uematsu, Nobuhiko ; Ogawa, Koji ; Tokinaga, Yasuyuki ; Tange, Kazuaki ; Hatano, Yoshio</creatorcontrib><description>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
< 0.05) in SHR than in WKY at the highest concentration of sevoflurane (5.1%). Y27632 (3 × 10
−7
M), 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 [Ca
2+
]
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
< 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.</description><identifier>ISSN: 0913-8668</identifier><identifier>EISSN: 1438-8359</identifier><identifier>DOI: 10.1007/s00540-011-1121-8</identifier><identifier>PMID: 21409351</identifier><language>eng</language><publisher>Japan: Springer Japan</publisher><subject>Amides - pharmacology ; Anesthesiology ; Anesthetics ; Anesthetics, Inhalation - pharmacology ; Angiotensin ; Angiotensin II - antagonists & inhibitors ; Angiotensin II - pharmacology ; Animals ; Aorta, Thoracic - drug effects ; Blood Pressure - drug effects ; Calcium - metabolism ; Calcium Signaling - drug effects ; Critical Care Medicine ; Emergency Medicine ; Enzyme Inhibitors - pharmacology ; Hypertension ; In Vitro Techniques ; Intensive ; Isometric Contraction - drug effects ; Male ; Medicine ; Medicine & Public Health ; Methyl Ethers - pharmacology ; Muscle Contraction - drug effects ; Muscle, Smooth, Vascular - drug effects ; Original Article ; Pain Medicine ; Protein Transport ; Pyridines - pharmacology ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; rho-Associated Kinases - antagonists & inhibitors ; Sevoflurane ; Smooth muscle</subject><ispartof>Journal of anesthesia, 2011-06, Vol.25 (3), p.398-404</ispartof><rights>Japanese Society of Anesthesiologists 2011</rights><rights>COPYRIGHT 2011 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c567t-8a434c4fa6f76cbba3b502c77b65038e0794e34b143da0b68420a1aedcafd2ca3</citedby><cites>FETCH-LOGICAL-c567t-8a434c4fa6f76cbba3b502c77b65038e0794e34b143da0b68420a1aedcafd2ca3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21409351$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Uematsu, Nobuhiko</creatorcontrib><creatorcontrib>Ogawa, Koji</creatorcontrib><creatorcontrib>Tokinaga, Yasuyuki</creatorcontrib><creatorcontrib>Tange, Kazuaki</creatorcontrib><creatorcontrib>Hatano, Yoshio</creatorcontrib><title>Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat</title><title>Journal of anesthesia</title><addtitle>J Anesth</addtitle><addtitle>J Anesth</addtitle><description>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
< 0.05) in SHR than in WKY at the highest concentration of sevoflurane (5.1%). Y27632 (3 × 10
−7
M), 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 [Ca
2+
]
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
< 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.</description><subject>Amides - pharmacology</subject><subject>Anesthesiology</subject><subject>Anesthetics</subject><subject>Anesthetics, Inhalation - pharmacology</subject><subject>Angiotensin</subject><subject>Angiotensin II - antagonists & inhibitors</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Blood Pressure - drug effects</subject><subject>Calcium - metabolism</subject><subject>Calcium Signaling - drug effects</subject><subject>Critical Care Medicine</subject><subject>Emergency Medicine</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Hypertension</subject><subject>In Vitro Techniques</subject><subject>Intensive</subject><subject>Isometric Contraction - drug effects</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Methyl Ethers - pharmacology</subject><subject>Muscle Contraction - drug effects</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Original Article</subject><subject>Pain Medicine</subject><subject>Protein Transport</subject><subject>Pyridines - pharmacology</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>rho-Associated Kinases - antagonists & inhibitors</subject><subject>Sevoflurane</subject><subject>Smooth muscle</subject><issn>0913-8668</issn><issn>1438-8359</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNp9kk2LFDEQhoMo7rj6A7xIwIOnrPnqdOa4LOoOLAh-nEM6XZnJ2p2MSffA_IT912bsVRAGySFQed6qVNWL0GtGrxil7ftCaSMpoYwRxjgj-glaMSk00aJZP0UrumaCaKX0BXpRyj2lVDEmnqMLziRdi4at0MNXOCQ_zNlGwCHuQhemgm3chjRBLCHizYaE2M8Oevxll_CPEG0BMkIf7FRjLsUpWzeFFHHy-GCLmwebcRlTmnZ4nIsbAPucRlz2la110lyGI94d95B_1zgAznZ6iZ55OxR49Xhfou8fP3y7uSV3nz9tbq7viGtUOxFtpZBOeqt8q1zXWdE1lLu27VRDhQbariUI2dU59JZ2SktOLbPQO-t77qy4RO-WvPucfs5QJjOG4mAYlp8Z3TKhFae8km8XcmsHMCH6dOr0RJtr0SgmOeOiUuQMtYUI2Q4pgg81_A9_dYavp4cxuLMCtghcTqVk8Gafw2jz0TBqTj4wiw9M9YE5-cDoqnnz2OTc1VX9VfxZfAX4ApT6FLeQzX2ac6yD_0_WX-TIv5Y</recordid><startdate>20110601</startdate><enddate>20110601</enddate><creator>Uematsu, Nobuhiko</creator><creator>Ogawa, Koji</creator><creator>Tokinaga, Yasuyuki</creator><creator>Tange, Kazuaki</creator><creator>Hatano, Yoshio</creator><general>Springer Japan</general><general>Springer</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20110601</creationdate><title>Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat</title><author>Uematsu, Nobuhiko ; Ogawa, Koji ; Tokinaga, Yasuyuki ; Tange, Kazuaki ; Hatano, Yoshio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c567t-8a434c4fa6f76cbba3b502c77b65038e0794e34b143da0b68420a1aedcafd2ca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Amides - pharmacology</topic><topic>Anesthesiology</topic><topic>Anesthetics</topic><topic>Anesthetics, Inhalation - pharmacology</topic><topic>Angiotensin</topic><topic>Angiotensin II - antagonists & inhibitors</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Aorta, Thoracic - drug effects</topic><topic>Blood Pressure - drug effects</topic><topic>Calcium - metabolism</topic><topic>Calcium Signaling - drug effects</topic><topic>Critical Care Medicine</topic><topic>Emergency Medicine</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Hypertension</topic><topic>In Vitro Techniques</topic><topic>Intensive</topic><topic>Isometric Contraction - drug effects</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Methyl Ethers - pharmacology</topic><topic>Muscle Contraction - drug effects</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Original Article</topic><topic>Pain Medicine</topic><topic>Protein Transport</topic><topic>Pyridines - pharmacology</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>rho-Associated Kinases - antagonists & inhibitors</topic><topic>Sevoflurane</topic><topic>Smooth muscle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Uematsu, Nobuhiko</creatorcontrib><creatorcontrib>Ogawa, Koji</creatorcontrib><creatorcontrib>Tokinaga, Yasuyuki</creatorcontrib><creatorcontrib>Tange, Kazuaki</creatorcontrib><creatorcontrib>Hatano, Yoshio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of anesthesia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Uematsu, Nobuhiko</au><au>Ogawa, Koji</au><au>Tokinaga, Yasuyuki</au><au>Tange, Kazuaki</au><au>Hatano, Yoshio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat</atitle><jtitle>Journal of anesthesia</jtitle><stitle>J Anesth</stitle><addtitle>J Anesth</addtitle><date>2011-06-01</date><risdate>2011</risdate><volume>25</volume><issue>3</issue><spage>398</spage><epage>404</epage><pages>398-404</pages><issn>0913-8668</issn><eissn>1438-8359</eissn><abstract>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
< 0.05) in SHR than in WKY at the highest concentration of sevoflurane (5.1%). Y27632 (3 × 10
−7
M), 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 [Ca
2+
]
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
< 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.</abstract><cop>Japan</cop><pub>Springer Japan</pub><pmid>21409351</pmid><doi>10.1007/s00540-011-1121-8</doi><tpages>7</tpages></addata></record> |
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| ispartof | Journal of anesthesia, 2011-06, Vol.25 (3), p.398-404 |
| issn | 0913-8668 1438-8359 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_871386202 |
| source | Springer Link |
| subjects | Amides - pharmacology Anesthesiology Anesthetics Anesthetics, Inhalation - pharmacology Angiotensin Angiotensin II - antagonists & inhibitors Angiotensin II - pharmacology Animals Aorta, Thoracic - drug effects Blood Pressure - drug effects Calcium - metabolism Calcium Signaling - drug effects Critical Care Medicine Emergency Medicine Enzyme Inhibitors - pharmacology Hypertension In Vitro Techniques Intensive Isometric Contraction - drug effects Male Medicine Medicine & Public Health Methyl Ethers - pharmacology Muscle Contraction - drug effects Muscle, Smooth, Vascular - drug effects Original Article Pain Medicine Protein Transport Pyridines - pharmacology Rats Rats, Inbred SHR Rats, Inbred WKY rho-Associated Kinases - antagonists & inhibitors Sevoflurane Smooth muscle |
| title | Sevoflurane inhibits angiotensin II-induced Rho kinase-mediated contraction of vascular smooth muscle from spontaneously hypertensive rat |
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