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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...
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Published in: | Biochemical pharmacology 2009-08, Vol.78 (4), p.374-381 |
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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 |
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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 & 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&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 & 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 & 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> |
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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 |
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