Microvascular responses to endothelin in deoxycorticosterone acetate-salt hypertensive rats
The objective of the present study was to determine if endothelin-1 played a role in the elevated peripheral resistance in deoxycorticosterone-acetate (DOCA)-salt hypertension. Radioimmunoassay showed that the concentration of endothelin-1 was higher in thoracic aorta of the DOCA-salt group than tha...
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| Veröffentlicht in: | American journal of hypertension 2000-07, Vol.13 (7), p.819-826 |
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| creator | Zhao, Hongli Joshua, Irving G Porter, James P |
| description | The objective of the present study was to determine if endothelin-1 played a role in the elevated peripheral resistance in deoxycorticosterone-acetate (DOCA)-salt hypertension. Radioimmunoassay showed that the concentration of endothelin-1 was higher in thoracic aorta of the DOCA-salt group than that of the control normotensive (CN) group. Responses of arterioles in the rat cremaster to endothelin-1 were also observed using in vivo closed circuit television microscopy. Microvascular sensitivity to endothelin-1 was decreased in the DOCA-salt group. In the presence of an endothelin type A (ET-A) receptor antagonist, low concentrations of endothelin-1 induced a significant vasoconstriction in the DOCA-salt group. In the presence of endothelin type B (ET-B) receptor antagonist, microvascular responses to endothelin-1 were attenuated in the DOCA-salt group. These results indicated that the increased tissue level of endothelin-1 may decrease the ET-A receptor-mediated vascular response to endothelin-1. However, the ET-B receptor-mediated vasoconstriction is potentiated during DOCA-salt hypertension. |
| doi_str_mv | 10.1016/S0895-7061(00)00260-0 |
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Radioimmunoassay showed that the concentration of endothelin-1 was higher in thoracic aorta of the DOCA-salt group than that of the control normotensive (CN) group. Responses of arterioles in the rat cremaster to endothelin-1 were also observed using in vivo closed circuit television microscopy. Microvascular sensitivity to endothelin-1 was decreased in the DOCA-salt group. In the presence of an endothelin type A (ET-A) receptor antagonist, low concentrations of endothelin-1 induced a significant vasoconstriction in the DOCA-salt group. In the presence of endothelin type B (ET-B) receptor antagonist, microvascular responses to endothelin-1 were attenuated in the DOCA-salt group. These results indicated that the increased tissue level of endothelin-1 may decrease the ET-A receptor-mediated vascular response to endothelin-1. However, the ET-B receptor-mediated vasoconstriction is potentiated during DOCA-salt hypertension.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1879-1905</identifier><identifier>EISSN: 1941-7225</identifier><identifier>DOI: 10.1016/S0895-7061(00)00260-0</identifier><identifier>PMID: 10933575</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Aorta, Thoracic ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Desoxycorticosterone ; DOCA-salt hypertension ; Dose-Response Relationship, Drug ; endothelin antagonist ; Endothelin Receptor Antagonists ; Endothelin-1 ; Endothelin-1 - blood ; Endothelin-1 - pharmacology ; Experimental diseases ; Hypertension - chemically induced ; Hypertension - physiopathology ; Male ; Medical sciences ; microcirculation ; Microcirculation - drug effects ; Muscle, Skeletal - blood supply ; Oligopeptides - pharmacology ; Peptides, Cyclic - pharmacology ; Piperidines - pharmacology ; rat ; Rats ; Rats, Sprague-Dawley ; Receptor, Endothelin A ; Receptor, Endothelin B ; Sodium Chloride</subject><ispartof>American journal of hypertension, 2000-07, Vol.13 (7), p.819-826</ispartof><rights>2000 American Journal of Hypertension, Ltd.</rights><rights>American Journal of Hypertension, Ltd. © 2000 by the American Journal of Hypertension, Ltd. 2000</rights><rights>2000 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jul 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c544t-7769c51aa67f10b06ae16cc2eebb7122716c15a51cbc4a6ce0f3fbb2c3d894d3</citedby><cites>FETCH-LOGICAL-c544t-7769c51aa67f10b06ae16cc2eebb7122716c15a51cbc4a6ce0f3fbb2c3d894d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1436969$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10933575$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Hongli</creatorcontrib><creatorcontrib>Joshua, Irving G</creatorcontrib><creatorcontrib>Porter, James P</creatorcontrib><title>Microvascular responses to endothelin in deoxycorticosterone acetate-salt hypertensive rats</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>The objective of the present study was to determine if endothelin-1 played a role in the elevated peripheral resistance in deoxycorticosterone-acetate (DOCA)-salt hypertension. Radioimmunoassay showed that the concentration of endothelin-1 was higher in thoracic aorta of the DOCA-salt group than that of the control normotensive (CN) group. Responses of arterioles in the rat cremaster to endothelin-1 were also observed using in vivo closed circuit television microscopy. Microvascular sensitivity to endothelin-1 was decreased in the DOCA-salt group. In the presence of an endothelin type A (ET-A) receptor antagonist, low concentrations of endothelin-1 induced a significant vasoconstriction in the DOCA-salt group. In the presence of endothelin type B (ET-B) receptor antagonist, microvascular responses to endothelin-1 were attenuated in the DOCA-salt group. These results indicated that the increased tissue level of endothelin-1 may decrease the ET-A receptor-mediated vascular response to endothelin-1. However, the ET-B receptor-mediated vasoconstriction is potentiated during DOCA-salt hypertension.</description><subject>Animals</subject><subject>Aorta, Thoracic</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Desoxycorticosterone</subject><subject>DOCA-salt hypertension</subject><subject>Dose-Response Relationship, Drug</subject><subject>endothelin antagonist</subject><subject>Endothelin Receptor Antagonists</subject><subject>Endothelin-1</subject><subject>Endothelin-1 - blood</subject><subject>Endothelin-1 - pharmacology</subject><subject>Experimental diseases</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>microcirculation</subject><subject>Microcirculation - drug effects</subject><subject>Muscle, Skeletal - blood supply</subject><subject>Oligopeptides - pharmacology</subject><subject>Peptides, Cyclic - pharmacology</subject><subject>Piperidines - pharmacology</subject><subject>rat</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Endothelin A</subject><subject>Receptor, Endothelin B</subject><subject>Sodium Chloride</subject><issn>0895-7061</issn><issn>1879-1905</issn><issn>1941-7225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkNFqFDEUhoModq0-gjJQL_QiejIzSXauSll0V6gU2oVKvQiZzBmaOp1Mk8zSfXuznaUqFITAIfD95-d8hLxl8IkBE58vYF5xKkGwDwAfAXIBFJ6RGZvLirIK-HMye0QOyKsQbgCgFIK9JAcMqqLgks_Iz-_WeLfRwYyd9pnHMLg-YMiiy7BvXLzGzvZZeg26-61xPlrjQkTvesy0wagj0qC7mF1vB_QR-2A3mHkdw2vyotVdwDf7eUjWX7-sFyt6erb8tjg5pYaXZaRSispwprWQLYMahEYmjMkR61qyPJfpx7jmzNSm1MIgtEVb17kpmnlVNsUhOZrWDt7djRiiunGj71OjYkmLyCUUMlF8otK5IXhs1eDtrfbbBKmdUfVgVO10KQD1YFRByr3bbx_rW2z-Sk0KE_B-DySJumu97o0Nf7iyEJWoEgYT5sbh6Wr6TzXdVdMpYpPv-8eQ9r-UkIXkavXjSi3P4XK5WF2pdeKPJx6T7I1Fr4Kx2BtsrEcTVePsf479DS2OsWA</recordid><startdate>20000701</startdate><enddate>20000701</enddate><creator>Zhao, Hongli</creator><creator>Joshua, Irving G</creator><creator>Porter, James P</creator><general>Elsevier Inc</general><general>Oxford University Press</general><general>Elsevier Science</general><scope>BSCLL</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20000701</creationdate><title>Microvascular responses to endothelin in deoxycorticosterone acetate-salt hypertensive rats</title><author>Zhao, Hongli ; Joshua, Irving G ; Porter, James P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c544t-7769c51aa67f10b06ae16cc2eebb7122716c15a51cbc4a6ce0f3fbb2c3d894d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Aorta, Thoracic</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Desoxycorticosterone</topic><topic>DOCA-salt hypertension</topic><topic>Dose-Response Relationship, Drug</topic><topic>endothelin antagonist</topic><topic>Endothelin Receptor Antagonists</topic><topic>Endothelin-1</topic><topic>Endothelin-1 - blood</topic><topic>Endothelin-1 - pharmacology</topic><topic>Experimental diseases</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>microcirculation</topic><topic>Microcirculation - drug effects</topic><topic>Muscle, Skeletal - blood supply</topic><topic>Oligopeptides - pharmacology</topic><topic>Peptides, Cyclic - pharmacology</topic><topic>Piperidines - pharmacology</topic><topic>rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Endothelin A</topic><topic>Receptor, Endothelin B</topic><topic>Sodium Chloride</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Hongli</creatorcontrib><creatorcontrib>Joshua, Irving G</creatorcontrib><creatorcontrib>Porter, James P</creatorcontrib><collection>Istex</collection><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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Hongli</au><au>Joshua, Irving G</au><au>Porter, James P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Microvascular responses to endothelin in deoxycorticosterone acetate-salt hypertensive rats</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2000-07-01</date><risdate>2000</risdate><volume>13</volume><issue>7</issue><spage>819</spage><epage>826</epage><pages>819-826</pages><issn>0895-7061</issn><eissn>1879-1905</eissn><eissn>1941-7225</eissn><coden>AJHYE6</coden><abstract>The objective of the present study was to determine if endothelin-1 played a role in the elevated peripheral resistance in deoxycorticosterone-acetate (DOCA)-salt hypertension. Radioimmunoassay showed that the concentration of endothelin-1 was higher in thoracic aorta of the DOCA-salt group than that of the control normotensive (CN) group. Responses of arterioles in the rat cremaster to endothelin-1 were also observed using in vivo closed circuit television microscopy. Microvascular sensitivity to endothelin-1 was decreased in the DOCA-salt group. In the presence of an endothelin type A (ET-A) receptor antagonist, low concentrations of endothelin-1 induced a significant vasoconstriction in the DOCA-salt group. In the presence of endothelin type B (ET-B) receptor antagonist, microvascular responses to endothelin-1 were attenuated in the DOCA-salt group. These results indicated that the increased tissue level of endothelin-1 may decrease the ET-A receptor-mediated vascular response to endothelin-1. However, the ET-B receptor-mediated vasoconstriction is potentiated during DOCA-salt hypertension.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10933575</pmid><doi>10.1016/S0895-7061(00)00260-0</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0895-7061 |
| ispartof | American journal of hypertension, 2000-07, Vol.13 (7), p.819-826 |
| issn | 0895-7061 1879-1905 1941-7225 |
| language | eng |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Aorta, Thoracic Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Desoxycorticosterone DOCA-salt hypertension Dose-Response Relationship, Drug endothelin antagonist Endothelin Receptor Antagonists Endothelin-1 Endothelin-1 - blood Endothelin-1 - pharmacology Experimental diseases Hypertension - chemically induced Hypertension - physiopathology Male Medical sciences microcirculation Microcirculation - drug effects Muscle, Skeletal - blood supply Oligopeptides - pharmacology Peptides, Cyclic - pharmacology Piperidines - pharmacology rat Rats Rats, Sprague-Dawley Receptor, Endothelin A Receptor, Endothelin B Sodium Chloride |
| title | Microvascular responses to endothelin in deoxycorticosterone acetate-salt hypertensive rats |
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