Loading…

Thromboxane prostanoid receptor activation impairs endothelial nitric oxide-dependent vasorelaxations: The role of Rho kinase

Activation of thromboxane prostanoid (TP) receptors causes potent vasoconstriction, which contributes to increased vascular tone and blood pressure. The present study examined the hypothesis that stimulation of TP receptor impaired endothelial nitric oxide-mediated vasorelaxation via a Rho kinase-de...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical pharmacology 2009-08, Vol.78 (4), p.374-381
Main Authors: Liu, Cui Qing, Leung, Fung Ping, Wong, Siu Ling, Wong, Wing Tak, Lau, Chi Wai, Lu, Limin, Yao, Xiaoqiang, Yao, Tai, Huang, Yu
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c447t-c8d5d1ba02d0ed95d7f56b010eb63f5a29f0246169fc13de8138277bb2f1a2123
cites cdi_FETCH-LOGICAL-c447t-c8d5d1ba02d0ed95d7f56b010eb63f5a29f0246169fc13de8138277bb2f1a2123
container_end_page 381
container_issue 4
container_start_page 374
container_title Biochemical pharmacology
container_volume 78
creator Liu, Cui Qing
Leung, Fung Ping
Wong, Siu Ling
Wong, Wing Tak
Lau, Chi Wai
Lu, Limin
Yao, Xiaoqiang
Yao, Tai
Huang, Yu
description Activation of thromboxane prostanoid (TP) receptors causes potent vasoconstriction, which contributes to increased vascular tone and blood pressure. The present study examined the hypothesis that stimulation of TP receptor impaired endothelial nitric oxide-mediated vasorelaxation via a Rho kinase-dependent mechanism. The common carotid arteries of Sprague–Dawley rats were isolated and suspended in myograph for measurement of changes in isometric tension. The production of nitric oxide in primary cultured aortic endothelial cells was assayed with an imaging technique and phosphorylated levels of endothelial NOS were determined by Western blot analysis. 9,11-dideoxy-11α,9α-epoxy-methanoprostaglandin F 2α (U46619) inhibited isoprenaline-induced relaxations in rings with or without endothelium. Treatment with Rho kinase inhibitors, Y27632 (2 μM) or HA 1077 (10 μM) prevented the effect of U46619 only in rings with endothelium while protein kinase C inhibitors were without effect. Rho kinase inhibitors did not affect isoprenaline-induced relaxations in endothelium-intact rings treated with L-NAME or 1H-[1,2,4]oxadizolo[4,3-a]quinoxalin-1-one (ODQ). Isoprenaline stimulated rises in nitric oxide (NO) production in cultured rat endothelial cells. The increased NO production was inhibited by U46619 (100 nM) and this effect was prevented by treatment with Y27632 but unaffected by the absence of extracellular calcium ions. U46619 attenuated isoprenaline-stimulated phosphorylation of eNOS, which was sensitive to inhibition by Y27632 and HA 1077. U46619-mediated effects were abolished by TP receptor antagonist, S18886 and the TP receptor was present in endothelial cells. The present results demonstrate that Rho kinase activation is likely to be the primary mechanism that underlies the U46619-stimulated TP-receptor-mediated inhibition of endothelial NO production and subsequent endothelium-dependent relaxations to isoprenaline.
doi_str_mv 10.1016/j.bcp.2009.04.022
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67394358</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006295209003049</els_id><sourcerecordid>67394358</sourcerecordid><originalsourceid>FETCH-LOGICAL-c447t-c8d5d1ba02d0ed95d7f56b010eb63f5a29f0246169fc13de8138277bb2f1a2123</originalsourceid><addsrcrecordid>eNp9kU2v1CAUhonReMerP8CNYaO7Vj5aWnRlbvxKbmJixjWhcMgwtlCBmYwL_7uMM9GdKw7heU84z0HoOSUtJVS83reTWVtGiGxJ1xLGHqANHQfeMCnGh2hDCBG17tkNepLz_nwdBX2MbqjsiOQD36Bf212KyxRPOgBeU8xFh-gtTmBgLTFhbYo_6uJjwH5ZtU8ZQ7Cx7GD2esbBl-QNjidvobGw1jcIBR91jglmffqTzG_wdgc4xRlwdPjrLuLvPugMT9Ejp-cMz67nLfr24f327lNz_-Xj57t3943puqE0ZrS9pZMmzBKwsreD68VEKIFJcNdrJh1hnaBCOkO5hZHykQ3DNDFHNaOM36JXl751wh8HyEUtPhuY5zp1PGQlBi473o8VpBfQVBU5gVNr8otOPxUl6uxc7VV1rs7OFelUdV4zL67ND9MC9l_iKrkCL6-AzkbPLulgfP7LMToQKWhfubcXDqqKo4eksvEQDFhf11GUjf4_3_gNmJWhtw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67394358</pqid></control><display><type>article</type><title>Thromboxane prostanoid receptor activation impairs endothelial nitric oxide-dependent vasorelaxations: The role of Rho kinase</title><source>Elsevier:Jisc Collections:Elsevier Read and Publish Agreement 2022-2024:Freedom Collection (Reading list)</source><creator>Liu, Cui Qing ; Leung, Fung Ping ; Wong, Siu Ling ; Wong, Wing Tak ; Lau, Chi Wai ; Lu, Limin ; Yao, Xiaoqiang ; Yao, Tai ; Huang, Yu</creator><creatorcontrib>Liu, Cui Qing ; Leung, Fung Ping ; Wong, Siu Ling ; Wong, Wing Tak ; Lau, Chi Wai ; Lu, Limin ; Yao, Xiaoqiang ; Yao, Tai ; Huang, Yu</creatorcontrib><description>Activation of thromboxane prostanoid (TP) receptors causes potent vasoconstriction, which contributes to increased vascular tone and blood pressure. The present study examined the hypothesis that stimulation of TP receptor impaired endothelial nitric oxide-mediated vasorelaxation via a Rho kinase-dependent mechanism. The common carotid arteries of Sprague–Dawley rats were isolated and suspended in myograph for measurement of changes in isometric tension. The production of nitric oxide in primary cultured aortic endothelial cells was assayed with an imaging technique and phosphorylated levels of endothelial NOS were determined by Western blot analysis. 9,11-dideoxy-11α,9α-epoxy-methanoprostaglandin F 2α (U46619) inhibited isoprenaline-induced relaxations in rings with or without endothelium. Treatment with Rho kinase inhibitors, Y27632 (2 μM) or HA 1077 (10 μM) prevented the effect of U46619 only in rings with endothelium while protein kinase C inhibitors were without effect. Rho kinase inhibitors did not affect isoprenaline-induced relaxations in endothelium-intact rings treated with L-NAME or 1H-[1,2,4]oxadizolo[4,3-a]quinoxalin-1-one (ODQ). Isoprenaline stimulated rises in nitric oxide (NO) production in cultured rat endothelial cells. The increased NO production was inhibited by U46619 (100 nM) and this effect was prevented by treatment with Y27632 but unaffected by the absence of extracellular calcium ions. U46619 attenuated isoprenaline-stimulated phosphorylation of eNOS, which was sensitive to inhibition by Y27632 and HA 1077. U46619-mediated effects were abolished by TP receptor antagonist, S18886 and the TP receptor was present in endothelial cells. The present results demonstrate that Rho kinase activation is likely to be the primary mechanism that underlies the U46619-stimulated TP-receptor-mediated inhibition of endothelial NO production and subsequent endothelium-dependent relaxations to isoprenaline.</description><identifier>ISSN: 0006-2952</identifier><identifier>EISSN: 1873-2968</identifier><identifier>DOI: 10.1016/j.bcp.2009.04.022</identifier><identifier>PMID: 19409373</identifier><identifier>CODEN: BCPCA6</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology ; Animals ; Biological and medical sciences ; Bronchodilator Agents - pharmacology ; Carotid artery ; Endothelium ; Endothelium - drug effects ; Endothelium - physiology ; Enzyme Inhibitors - pharmacology ; Isoprenaline ; Isoproterenol - pharmacology ; Medical sciences ; Muscle Relaxation ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric oxide ; Nitric Oxide - physiology ; Nitric Oxide Synthase Type III ; Pharmacology. Drug treatments ; Rats ; Rats, Sprague-Dawley ; Rho kinase ; rho-Associated Kinases - antagonists &amp; inhibitors ; rho-Associated Kinases - physiology ; TP receptor ; Vasoconstrictor Agents - pharmacology ; Vasodilation - drug effects ; Vasodilation - physiology ; Vasodilator Agents - pharmacology</subject><ispartof>Biochemical pharmacology, 2009-08, Vol.78 (4), p.374-381</ispartof><rights>2009 Elsevier Inc.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-c8d5d1ba02d0ed95d7f56b010eb63f5a29f0246169fc13de8138277bb2f1a2123</citedby><cites>FETCH-LOGICAL-c447t-c8d5d1ba02d0ed95d7f56b010eb63f5a29f0246169fc13de8138277bb2f1a2123</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=21709615$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19409373$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Cui Qing</creatorcontrib><creatorcontrib>Leung, Fung Ping</creatorcontrib><creatorcontrib>Wong, Siu Ling</creatorcontrib><creatorcontrib>Wong, Wing Tak</creatorcontrib><creatorcontrib>Lau, Chi Wai</creatorcontrib><creatorcontrib>Lu, Limin</creatorcontrib><creatorcontrib>Yao, Xiaoqiang</creatorcontrib><creatorcontrib>Yao, Tai</creatorcontrib><creatorcontrib>Huang, Yu</creatorcontrib><title>Thromboxane prostanoid receptor activation impairs endothelial nitric oxide-dependent vasorelaxations: The role of Rho kinase</title><title>Biochemical pharmacology</title><addtitle>Biochem Pharmacol</addtitle><description>Activation of thromboxane prostanoid (TP) receptors causes potent vasoconstriction, which contributes to increased vascular tone and blood pressure. The present study examined the hypothesis that stimulation of TP receptor impaired endothelial nitric oxide-mediated vasorelaxation via a Rho kinase-dependent mechanism. The common carotid arteries of Sprague–Dawley rats were isolated and suspended in myograph for measurement of changes in isometric tension. The production of nitric oxide in primary cultured aortic endothelial cells was assayed with an imaging technique and phosphorylated levels of endothelial NOS were determined by Western blot analysis. 9,11-dideoxy-11α,9α-epoxy-methanoprostaglandin F 2α (U46619) inhibited isoprenaline-induced relaxations in rings with or without endothelium. Treatment with Rho kinase inhibitors, Y27632 (2 μM) or HA 1077 (10 μM) prevented the effect of U46619 only in rings with endothelium while protein kinase C inhibitors were without effect. Rho kinase inhibitors did not affect isoprenaline-induced relaxations in endothelium-intact rings treated with L-NAME or 1H-[1,2,4]oxadizolo[4,3-a]quinoxalin-1-one (ODQ). Isoprenaline stimulated rises in nitric oxide (NO) production in cultured rat endothelial cells. The increased NO production was inhibited by U46619 (100 nM) and this effect was prevented by treatment with Y27632 but unaffected by the absence of extracellular calcium ions. U46619 attenuated isoprenaline-stimulated phosphorylation of eNOS, which was sensitive to inhibition by Y27632 and HA 1077. U46619-mediated effects were abolished by TP receptor antagonist, S18886 and the TP receptor was present in endothelial cells. The present results demonstrate that Rho kinase activation is likely to be the primary mechanism that underlies the U46619-stimulated TP-receptor-mediated inhibition of endothelial NO production and subsequent endothelium-dependent relaxations to isoprenaline.</description><subject>15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bronchodilator Agents - pharmacology</subject><subject>Carotid artery</subject><subject>Endothelium</subject><subject>Endothelium - drug effects</subject><subject>Endothelium - physiology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Isoprenaline</subject><subject>Isoproterenol - pharmacology</subject><subject>Medical sciences</subject><subject>Muscle Relaxation</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rho kinase</subject><subject>rho-Associated Kinases - antagonists &amp; inhibitors</subject><subject>rho-Associated Kinases - physiology</subject><subject>TP receptor</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0006-2952</issn><issn>1873-2968</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNp9kU2v1CAUhonReMerP8CNYaO7Vj5aWnRlbvxKbmJixjWhcMgwtlCBmYwL_7uMM9GdKw7heU84z0HoOSUtJVS83reTWVtGiGxJ1xLGHqANHQfeMCnGh2hDCBG17tkNepLz_nwdBX2MbqjsiOQD36Bf212KyxRPOgBeU8xFh-gtTmBgLTFhbYo_6uJjwH5ZtU8ZQ7Cx7GD2esbBl-QNjidvobGw1jcIBR91jglmffqTzG_wdgc4xRlwdPjrLuLvPugMT9Ejp-cMz67nLfr24f327lNz_-Xj57t3943puqE0ZrS9pZMmzBKwsreD68VEKIFJcNdrJh1hnaBCOkO5hZHykQ3DNDFHNaOM36JXl751wh8HyEUtPhuY5zp1PGQlBi473o8VpBfQVBU5gVNr8otOPxUl6uxc7VV1rs7OFelUdV4zL67ND9MC9l_iKrkCL6-AzkbPLulgfP7LMToQKWhfubcXDqqKo4eksvEQDFhf11GUjf4_3_gNmJWhtw</recordid><startdate>20090815</startdate><enddate>20090815</enddate><creator>Liu, Cui Qing</creator><creator>Leung, Fung Ping</creator><creator>Wong, Siu Ling</creator><creator>Wong, Wing Tak</creator><creator>Lau, Chi Wai</creator><creator>Lu, Limin</creator><creator>Yao, Xiaoqiang</creator><creator>Yao, Tai</creator><creator>Huang, Yu</creator><general>Elsevier Inc</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>7X8</scope></search><sort><creationdate>20090815</creationdate><title>Thromboxane prostanoid receptor activation impairs endothelial nitric oxide-dependent vasorelaxations: The role of Rho kinase</title><author>Liu, Cui Qing ; Leung, Fung Ping ; Wong, Siu Ling ; Wong, Wing Tak ; Lau, Chi Wai ; Lu, Limin ; Yao, Xiaoqiang ; Yao, Tai ; Huang, Yu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-c8d5d1ba02d0ed95d7f56b010eb63f5a29f0246169fc13de8138277bb2f1a2123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bronchodilator Agents - pharmacology</topic><topic>Carotid artery</topic><topic>Endothelium</topic><topic>Endothelium - drug effects</topic><topic>Endothelium - physiology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Isoprenaline</topic><topic>Isoproterenol - pharmacology</topic><topic>Medical sciences</topic><topic>Muscle Relaxation</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rho kinase</topic><topic>rho-Associated Kinases - antagonists &amp; inhibitors</topic><topic>rho-Associated Kinases - physiology</topic><topic>TP receptor</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Cui Qing</creatorcontrib><creatorcontrib>Leung, Fung Ping</creatorcontrib><creatorcontrib>Wong, Siu Ling</creatorcontrib><creatorcontrib>Wong, Wing Tak</creatorcontrib><creatorcontrib>Lau, Chi Wai</creatorcontrib><creatorcontrib>Lu, Limin</creatorcontrib><creatorcontrib>Yao, Xiaoqiang</creatorcontrib><creatorcontrib>Yao, Tai</creatorcontrib><creatorcontrib>Huang, Yu</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>MEDLINE - Academic</collection><jtitle>Biochemical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Cui Qing</au><au>Leung, Fung Ping</au><au>Wong, Siu Ling</au><au>Wong, Wing Tak</au><au>Lau, Chi Wai</au><au>Lu, Limin</au><au>Yao, Xiaoqiang</au><au>Yao, Tai</au><au>Huang, Yu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thromboxane prostanoid receptor activation impairs endothelial nitric oxide-dependent vasorelaxations: The role of Rho kinase</atitle><jtitle>Biochemical pharmacology</jtitle><addtitle>Biochem Pharmacol</addtitle><date>2009-08-15</date><risdate>2009</risdate><volume>78</volume><issue>4</issue><spage>374</spage><epage>381</epage><pages>374-381</pages><issn>0006-2952</issn><eissn>1873-2968</eissn><coden>BCPCA6</coden><abstract>Activation of thromboxane prostanoid (TP) receptors causes potent vasoconstriction, which contributes to increased vascular tone and blood pressure. The present study examined the hypothesis that stimulation of TP receptor impaired endothelial nitric oxide-mediated vasorelaxation via a Rho kinase-dependent mechanism. The common carotid arteries of Sprague–Dawley rats were isolated and suspended in myograph for measurement of changes in isometric tension. The production of nitric oxide in primary cultured aortic endothelial cells was assayed with an imaging technique and phosphorylated levels of endothelial NOS were determined by Western blot analysis. 9,11-dideoxy-11α,9α-epoxy-methanoprostaglandin F 2α (U46619) inhibited isoprenaline-induced relaxations in rings with or without endothelium. Treatment with Rho kinase inhibitors, Y27632 (2 μM) or HA 1077 (10 μM) prevented the effect of U46619 only in rings with endothelium while protein kinase C inhibitors were without effect. Rho kinase inhibitors did not affect isoprenaline-induced relaxations in endothelium-intact rings treated with L-NAME or 1H-[1,2,4]oxadizolo[4,3-a]quinoxalin-1-one (ODQ). Isoprenaline stimulated rises in nitric oxide (NO) production in cultured rat endothelial cells. The increased NO production was inhibited by U46619 (100 nM) and this effect was prevented by treatment with Y27632 but unaffected by the absence of extracellular calcium ions. U46619 attenuated isoprenaline-stimulated phosphorylation of eNOS, which was sensitive to inhibition by Y27632 and HA 1077. U46619-mediated effects were abolished by TP receptor antagonist, S18886 and the TP receptor was present in endothelial cells. The present results demonstrate that Rho kinase activation is likely to be the primary mechanism that underlies the U46619-stimulated TP-receptor-mediated inhibition of endothelial NO production and subsequent endothelium-dependent relaxations to isoprenaline.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>19409373</pmid><doi>10.1016/j.bcp.2009.04.022</doi><tpages>8</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0006-2952
ispartof Biochemical pharmacology, 2009-08, Vol.78 (4), p.374-381
issn 0006-2952
1873-2968
language eng
recordid cdi_proquest_miscellaneous_67394358
source Elsevier:Jisc Collections:Elsevier Read and Publish Agreement 2022-2024:Freedom Collection (Reading list)
subjects 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology
Animals
Biological and medical sciences
Bronchodilator Agents - pharmacology
Carotid artery
Endothelium
Endothelium - drug effects
Endothelium - physiology
Enzyme Inhibitors - pharmacology
Isoprenaline
Isoproterenol - pharmacology
Medical sciences
Muscle Relaxation
NG-Nitroarginine Methyl Ester - pharmacology
Nitric oxide
Nitric Oxide - physiology
Nitric Oxide Synthase Type III
Pharmacology. Drug treatments
Rats
Rats, Sprague-Dawley
Rho kinase
rho-Associated Kinases - antagonists & inhibitors
rho-Associated Kinases - physiology
TP receptor
Vasoconstrictor Agents - pharmacology
Vasodilation - drug effects
Vasodilation - physiology
Vasodilator Agents - pharmacology
title Thromboxane prostanoid receptor activation impairs endothelial nitric oxide-dependent vasorelaxations: The role of Rho kinase
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T12%3A04%3A11IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Thromboxane%20prostanoid%20receptor%20activation%20impairs%20endothelial%20nitric%20oxide-dependent%20vasorelaxations:%20The%20role%20of%20Rho%20kinase&rft.jtitle=Biochemical%20pharmacology&rft.au=Liu,%20Cui%20Qing&rft.date=2009-08-15&rft.volume=78&rft.issue=4&rft.spage=374&rft.epage=381&rft.pages=374-381&rft.issn=0006-2952&rft.eissn=1873-2968&rft.coden=BCPCA6&rft_id=info:doi/10.1016/j.bcp.2009.04.022&rft_dat=%3Cproquest_cross%3E67394358%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c447t-c8d5d1ba02d0ed95d7f56b010eb63f5a29f0246169fc13de8138277bb2f1a2123%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=67394358&rft_id=info:pmid/19409373&rfr_iscdi=true