Involvement of Rho-kinase in collar-induced vasoconstriction and vascular hypersensitivity to serotonin in rat carotid
Abstract Background Vasoconstriction and vascular hypersensitivity to serotonin has been described previously in animal models of adventitia injury. The present study was undertaken to investigate the contribution of the RhoA/Rho-kinase pathway to the collar-induced the change of vascular contractil...
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| description | Abstract Background Vasoconstriction and vascular hypersensitivity to serotonin has been described previously in animal models of adventitia injury. The present study was undertaken to investigate the contribution of the RhoA/Rho-kinase pathway to the collar-induced the change of vascular contractility and reactivity in rat carotid artery. Methods Wistar Kyoto rats were assigned to 4 treatments ( n = 12): vehicle, fasudil, valsartan, and fasudil plus valsartan. After 1 week of treatment, adventitia injury was induced by positioning a silicone collar around the right carotid artery for 1 week. Blood flow and vascular reactivity to serotonin was determined 1 week after injury, and carotids were harvested for morphometry and biochemical analysis. Results Adventitia injury leaded to histological changes of vasoconstriction with the percent lumen patency of 54.5 ± 4.3% ( p < 0.001) decreasing, accompanying by the reduction of the blood flow (2.79 ± 0.22 ml/min vs. 3.67 ± 0.26 mi/min， p < 0.001) when compared to contralateral arteries. The increase of vascular reactivity sensitivity to serotonin was observed in the collared artery when compared with the contralateral artery. Treatment with valsartan and fasudil prevented the development of vasoconstriction, improved the carotid blood flow and normalized the hypersensitivity to serotonin. Injury increased Angiotensin II type 1（AT1 ）receptor, Rho-kinase, and p-MYPT1Thr696 expression. Valsartan lowered the Rho-kinase and p-MYPT1Thr696 expression. Fasudil inhibited the p-MYPT1Thr696 expression. Conclusions Collar-induced adventitia injury resulted in the enhancement of vascular contractility and reactivity. The activation of RhoA/Rho-kinase signal pathway, stimulated by AT1 receptor, plays an important role in the collar-induced the change of vascular contractility and reactivity. |
| doi_str_mv | 10.1016/j.ijcard.2009.10.051 |
| format | Article |
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The present study was undertaken to investigate the contribution of the RhoA/Rho-kinase pathway to the collar-induced the change of vascular contractility and reactivity in rat carotid artery. Methods Wistar Kyoto rats were assigned to 4 treatments ( n = 12): vehicle, fasudil, valsartan, and fasudil plus valsartan. After 1 week of treatment, adventitia injury was induced by positioning a silicone collar around the right carotid artery for 1 week. Blood flow and vascular reactivity to serotonin was determined 1 week after injury, and carotids were harvested for morphometry and biochemical analysis. Results Adventitia injury leaded to histological changes of vasoconstriction with the percent lumen patency of 54.5 ± 4.3% ( p < 0.001) decreasing, accompanying by the reduction of the blood flow (2.79 ± 0.22 ml/min vs. 3.67 ± 0.26 mi/min， p < 0.001) when compared to contralateral arteries. The increase of vascular reactivity sensitivity to serotonin was observed in the collared artery when compared with the contralateral artery. Treatment with valsartan and fasudil prevented the development of vasoconstriction, improved the carotid blood flow and normalized the hypersensitivity to serotonin. Injury increased Angiotensin II type 1（AT1 ）receptor, Rho-kinase, and p-MYPT1Thr696 expression. Valsartan lowered the Rho-kinase and p-MYPT1Thr696 expression. Fasudil inhibited the p-MYPT1Thr696 expression. Conclusions Collar-induced adventitia injury resulted in the enhancement of vascular contractility and reactivity. The activation of RhoA/Rho-kinase signal pathway, stimulated by AT1 receptor, plays an important role in the collar-induced the change of vascular contractility and reactivity.</description><identifier>ISSN: 0167-5273</identifier><identifier>EISSN: 1874-1754</identifier><identifier>DOI: 10.1016/j.ijcard.2009.10.051</identifier><identifier>PMID: 19942308</identifier><identifier>CODEN: IJCDD5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives ; 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology ; Adventitia ; Angiotensin II ; Angiotensin II type 1 receptor ; Angiotensin II Type 1 Receptor Blockers - pharmacology ; Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Cardiovascular ; Carotid Artery Diseases - drug therapy ; Carotid Artery Diseases - metabolism ; Carotid Artery Diseases - physiopathology ; Cerebrovascular Circulation - drug effects ; Cerebrovascular Circulation - physiology ; Disease Models, Animal ; Male ; Medical sciences ; Protein Kinase Inhibitors - pharmacology ; Rats ; Rats, Inbred WKY ; Receptor, Angiotensin, Type 1 - metabolism ; rho-Associated Kinases - antagonists & inhibitors ; rho-Associated Kinases - metabolism ; Rho-kinase ; rhoA GTP-Binding Protein - metabolism ; Serotonin ; Serotonin - pharmacology ; Silicone collar ; Silicones ; Tetrazoles - pharmacology ; Valine - analogs & derivatives ; Valine - pharmacology ; Valsartan ; Vasoconstriction ; Vasoconstriction - drug effects ; Vasoconstriction - physiology</subject><ispartof>International journal of cardiology, 2011-04, Vol.148 (2), p.168-173</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2009 Elsevier Ireland Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c479t-6b20cce6c8818d2aa48d04d6e9d19246dcfcb4450fbdbc7754f30e3c34e3d14e3</citedby><cites>FETCH-LOGICAL-c479t-6b20cce6c8818d2aa48d04d6e9d19246dcfcb4450fbdbc7754f30e3c34e3d14e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ijcard.2009.10.051$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27913,27914,45984</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24037614$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19942308$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xie, Lianna</creatorcontrib><creatorcontrib>Zeng, Dingyin</creatorcontrib><creatorcontrib>Zhang, Haishan</creatorcontrib><creatorcontrib>Sun, Danmeng</creatorcontrib><creatorcontrib>Pang, Xuefeng</creatorcontrib><creatorcontrib>Guan, Qigang</creatorcontrib><title>Involvement of Rho-kinase in collar-induced vasoconstriction and vascular hypersensitivity to serotonin in rat carotid</title><title>International journal of cardiology</title><addtitle>Int J Cardiol</addtitle><description>Abstract Background Vasoconstriction and vascular hypersensitivity to serotonin has been described previously in animal models of adventitia injury. The present study was undertaken to investigate the contribution of the RhoA/Rho-kinase pathway to the collar-induced the change of vascular contractility and reactivity in rat carotid artery. Methods Wistar Kyoto rats were assigned to 4 treatments ( n = 12): vehicle, fasudil, valsartan, and fasudil plus valsartan. After 1 week of treatment, adventitia injury was induced by positioning a silicone collar around the right carotid artery for 1 week. Blood flow and vascular reactivity to serotonin was determined 1 week after injury, and carotids were harvested for morphometry and biochemical analysis. Results Adventitia injury leaded to histological changes of vasoconstriction with the percent lumen patency of 54.5 ± 4.3% ( p < 0.001) decreasing, accompanying by the reduction of the blood flow (2.79 ± 0.22 ml/min vs. 3.67 ± 0.26 mi/min， p < 0.001) when compared to contralateral arteries. The increase of vascular reactivity sensitivity to serotonin was observed in the collared artery when compared with the contralateral artery. Treatment with valsartan and fasudil prevented the development of vasoconstriction, improved the carotid blood flow and normalized the hypersensitivity to serotonin. Injury increased Angiotensin II type 1（AT1 ）receptor, Rho-kinase, and p-MYPT1Thr696 expression. Valsartan lowered the Rho-kinase and p-MYPT1Thr696 expression. Fasudil inhibited the p-MYPT1Thr696 expression. Conclusions Collar-induced adventitia injury resulted in the enhancement of vascular contractility and reactivity. The activation of RhoA/Rho-kinase signal pathway, stimulated by AT1 receptor, plays an important role in the collar-induced the change of vascular contractility and reactivity.</description><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives</subject><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology</subject><subject>Adventitia</subject><subject>Angiotensin II</subject><subject>Angiotensin II type 1 receptor</subject><subject>Angiotensin II Type 1 Receptor Blockers - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular</subject><subject>Carotid Artery Diseases - drug therapy</subject><subject>Carotid Artery Diseases - metabolism</subject><subject>Carotid Artery Diseases - physiopathology</subject><subject>Cerebrovascular Circulation - drug effects</subject><subject>Cerebrovascular Circulation - physiology</subject><subject>Disease Models, Animal</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Rats</subject><subject>Rats, Inbred WKY</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>rho-Associated Kinases - antagonists & inhibitors</subject><subject>rho-Associated Kinases - metabolism</subject><subject>Rho-kinase</subject><subject>rhoA GTP-Binding Protein - metabolism</subject><subject>Serotonin</subject><subject>Serotonin - pharmacology</subject><subject>Silicone collar</subject><subject>Silicones</subject><subject>Tetrazoles - pharmacology</subject><subject>Valine - analogs & derivatives</subject><subject>Valine - pharmacology</subject><subject>Valsartan</subject><subject>Vasoconstriction</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasoconstriction - physiology</subject><issn>0167-5273</issn><issn>1874-1754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFktuKFDEQhoMo7uzqG4j0jbg3PebUh9wIsnhYWBA8XId0Us1mticZk3TDvL3VzqDghUJIoPjqr8MfQl4wumWUtW92W7-zJrktp1RhaEsb9ohsWN_JmnWNfEw2iHV1wztxQS5z3lFKpVL9U3LBlJJc0H5DltuwxGmBPYRSxbH6ch_rBx9MhsqHysZpMqn2wc0WXLWYHG0MuSRvi4-hMuFX0M5IVffHA6QMIfviF1-OVYlVhhRLDCiFJ5lSYcexePeMPBnNlOH5-b0i3z-8_3bzqb77_PH25t1dbWWnSt0OnFoLre171jtujOwdla4F5ZjisnV2tIOUDR0HN9gOpx4FBWGFBOEYXlfk9Un3kOKPGXLRe58t4FQB4px13yjBuOgVktf_JJlssQ5vlUBUnlCbYs4JRn1Ifm_SUTOqV2_0Tp-80as3axS9wbSX5wrzsAf3J-lsBgKvzgCu1ExjMsH6_JvjkoquZRK5tycOcHOLh6Sz9RDQIZ_AFu2i_18nfwvYyQePNR_gCHkX5xTQFc105prqr-s_Wr8RVZQ1DQr8BArRxkY</recordid><startdate>20110414</startdate><enddate>20110414</enddate><creator>Xie, Lianna</creator><creator>Zeng, Dingyin</creator><creator>Zhang, Haishan</creator><creator>Sun, Danmeng</creator><creator>Pang, Xuefeng</creator><creator>Guan, Qigang</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20110414</creationdate><title>Involvement of Rho-kinase in collar-induced vasoconstriction and vascular hypersensitivity to serotonin in rat carotid</title><author>Xie, Lianna ; Zeng, Dingyin ; Zhang, Haishan ; Sun, Danmeng ; Pang, Xuefeng ; Guan, Qigang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c479t-6b20cce6c8818d2aa48d04d6e9d19246dcfcb4450fbdbc7754f30e3c34e3d14e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives</topic><topic>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology</topic><topic>Adventitia</topic><topic>Angiotensin II</topic><topic>Angiotensin II type 1 receptor</topic><topic>Angiotensin II Type 1 Receptor Blockers - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular</topic><topic>Carotid Artery Diseases - drug therapy</topic><topic>Carotid Artery Diseases - metabolism</topic><topic>Carotid Artery Diseases - physiopathology</topic><topic>Cerebrovascular Circulation - drug effects</topic><topic>Cerebrovascular Circulation - physiology</topic><topic>Disease Models, Animal</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Rats</topic><topic>Rats, Inbred WKY</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>rho-Associated Kinases - antagonists & inhibitors</topic><topic>rho-Associated Kinases - metabolism</topic><topic>Rho-kinase</topic><topic>rhoA GTP-Binding Protein - metabolism</topic><topic>Serotonin</topic><topic>Serotonin - pharmacology</topic><topic>Silicone collar</topic><topic>Silicones</topic><topic>Tetrazoles - pharmacology</topic><topic>Valine - analogs & derivatives</topic><topic>Valine - pharmacology</topic><topic>Valsartan</topic><topic>Vasoconstriction</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasoconstriction - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xie, Lianna</creatorcontrib><creatorcontrib>Zeng, Dingyin</creatorcontrib><creatorcontrib>Zhang, Haishan</creatorcontrib><creatorcontrib>Sun, Danmeng</creatorcontrib><creatorcontrib>Pang, Xuefeng</creatorcontrib><creatorcontrib>Guan, Qigang</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xie, Lianna</au><au>Zeng, Dingyin</au><au>Zhang, Haishan</au><au>Sun, Danmeng</au><au>Pang, Xuefeng</au><au>Guan, Qigang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of Rho-kinase in collar-induced vasoconstriction and vascular hypersensitivity to serotonin in rat carotid</atitle><jtitle>International journal of cardiology</jtitle><addtitle>Int J Cardiol</addtitle><date>2011-04-14</date><risdate>2011</risdate><volume>148</volume><issue>2</issue><spage>168</spage><epage>173</epage><pages>168-173</pages><issn>0167-5273</issn><eissn>1874-1754</eissn><coden>IJCDD5</coden><abstract>Abstract Background Vasoconstriction and vascular hypersensitivity to serotonin has been described previously in animal models of adventitia injury. The present study was undertaken to investigate the contribution of the RhoA/Rho-kinase pathway to the collar-induced the change of vascular contractility and reactivity in rat carotid artery. Methods Wistar Kyoto rats were assigned to 4 treatments ( n = 12): vehicle, fasudil, valsartan, and fasudil plus valsartan. After 1 week of treatment, adventitia injury was induced by positioning a silicone collar around the right carotid artery for 1 week. Blood flow and vascular reactivity to serotonin was determined 1 week after injury, and carotids were harvested for morphometry and biochemical analysis. Results Adventitia injury leaded to histological changes of vasoconstriction with the percent lumen patency of 54.5 ± 4.3% ( p < 0.001) decreasing, accompanying by the reduction of the blood flow (2.79 ± 0.22 ml/min vs. 3.67 ± 0.26 mi/min， p < 0.001) when compared to contralateral arteries. The increase of vascular reactivity sensitivity to serotonin was observed in the collared artery when compared with the contralateral artery. Treatment with valsartan and fasudil prevented the development of vasoconstriction, improved the carotid blood flow and normalized the hypersensitivity to serotonin. Injury increased Angiotensin II type 1（AT1 ）receptor, Rho-kinase, and p-MYPT1Thr696 expression. Valsartan lowered the Rho-kinase and p-MYPT1Thr696 expression. Fasudil inhibited the p-MYPT1Thr696 expression. Conclusions Collar-induced adventitia injury resulted in the enhancement of vascular contractility and reactivity. The activation of RhoA/Rho-kinase signal pathway, stimulated by AT1 receptor, plays an important role in the collar-induced the change of vascular contractility and reactivity.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>19942308</pmid><doi>10.1016/j.ijcard.2009.10.051</doi><tpages>6</tpages></addata></record> |
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| subjects | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology Adventitia Angiotensin II Angiotensin II type 1 receptor Angiotensin II Type 1 Receptor Blockers - pharmacology Animals Biological and medical sciences Cardiology. Vascular system Cardiovascular Carotid Artery Diseases - drug therapy Carotid Artery Diseases - metabolism Carotid Artery Diseases - physiopathology Cerebrovascular Circulation - drug effects Cerebrovascular Circulation - physiology Disease Models, Animal Male Medical sciences Protein Kinase Inhibitors - pharmacology Rats Rats, Inbred WKY Receptor, Angiotensin, Type 1 - metabolism rho-Associated Kinases - antagonists & inhibitors rho-Associated Kinases - metabolism Rho-kinase rhoA GTP-Binding Protein - metabolism Serotonin Serotonin - pharmacology Silicone collar Silicones Tetrazoles - pharmacology Valine - analogs & derivatives Valine - pharmacology Valsartan Vasoconstriction Vasoconstriction - drug effects Vasoconstriction - physiology |
| title | Involvement of Rho-kinase in collar-induced vasoconstriction and vascular hypersensitivity to serotonin in rat carotid |
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