Evidence for a new angiotensin-(1–7) receptor subtype in the aorta of Sprague–Dawley rats
We have recently described, in the mouse aorta, the vasodilator effect of angiotensin-(1–7) (Ang-(1–7)) was mediated by activation of the Mas Ang-(1–7) receptor and that A-779 and D-Pro 7-Ang-(1–7) act as Mas receptor antagonists. In this work we show pharmacological evidence for the existence of a...
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creator | Silva, D.M.R. Vianna, H.R. Cortes, S.F. Campagnole-Santos, M.J. Santos, R.A.S. Lemos, V.S. |
description | We have recently described, in the mouse aorta, the vasodilator effect of angiotensin-(1–7) (Ang-(1–7)) was mediated by activation of the Mas Ang-(1–7) receptor and that A-779 and D-Pro
7-Ang-(1–7) act as Mas receptor antagonists. In this work we show pharmacological evidence for the existence of a different Ang-(1–7) receptor subtype mediating the vasodilator effect of Ang-(1–7) in the aorta from Sprague–Dawley (SD) rats. Ang-(1–7) induced an endothelium-dependent vasodilator effect in aortic rings from SD rats which was inhibited by removal of the endothelium and by
l-NAME (100
μM) but not by indomethacin (10
μM). The Ang-(1–7) receptor antagonist D-Pro
7-Ang-(1–7) (0.1
μM) abolished the vasodilator effect of the peptide. However, the other specific Ang-(1–7) receptor antagonist, A-779 in concentrations up to 10
μM, did not affect vasodilation induced by Ang-(1–7). The Ang II AT
1 and AT
2 receptors antagonists CV11974 (0.01
μM) and PD123319 (1
μM), respectively, the bradykinin B
2 receptor antagonist HOE 140 (1
μM) and the inhibitor of ACE captopril (10
μM) did not change the effect of Ang-(1–7). Our results show that in the aorta of SD rats, the vasodilator effect of Ang-(1–7) is dependent on endothelium-derived nitric oxide. This effect is mediated by the activation of Ang-(1–7) receptors sensitive to D-Pro
7-Ang-(1–7), but not to A-779, which suggests the existence of a different Ang-(1–7) receptor subtype. |
doi_str_mv | 10.1016/j.peptides.2006.10.007 |
format | Article |
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7-Ang-(1–7) act as Mas receptor antagonists. In this work we show pharmacological evidence for the existence of a different Ang-(1–7) receptor subtype mediating the vasodilator effect of Ang-(1–7) in the aorta from Sprague–Dawley (SD) rats. Ang-(1–7) induced an endothelium-dependent vasodilator effect in aortic rings from SD rats which was inhibited by removal of the endothelium and by
l-NAME (100
μM) but not by indomethacin (10
μM). The Ang-(1–7) receptor antagonist D-Pro
7-Ang-(1–7) (0.1
μM) abolished the vasodilator effect of the peptide. However, the other specific Ang-(1–7) receptor antagonist, A-779 in concentrations up to 10
μM, did not affect vasodilation induced by Ang-(1–7). The Ang II AT
1 and AT
2 receptors antagonists CV11974 (0.01
μM) and PD123319 (1
μM), respectively, the bradykinin B
2 receptor antagonist HOE 140 (1
μM) and the inhibitor of ACE captopril (10
μM) did not change the effect of Ang-(1–7). Our results show that in the aorta of SD rats, the vasodilator effect of Ang-(1–7) is dependent on endothelium-derived nitric oxide. This effect is mediated by the activation of Ang-(1–7) receptors sensitive to D-Pro
7-Ang-(1–7), but not to A-779, which suggests the existence of a different Ang-(1–7) receptor subtype.</description><identifier>ISSN: 0196-9781</identifier><identifier>EISSN: 1873-5169</identifier><identifier>DOI: 10.1016/j.peptides.2006.10.007</identifier><identifier>PMID: 17129638</identifier><identifier>CODEN: PPTDD5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Ang-(1–7) ; Angiotensin I - antagonists & inhibitors ; Angiotensin I - metabolism ; Angiotensin I - pharmacology ; Angiotensin II - analogs & derivatives ; Angiotensin II - pharmacology ; Animals ; Aorta, Thoracic - drug effects ; Aorta, Thoracic - metabolism ; Aorta, Thoracic - physiology ; Biological and medical sciences ; Fundamental and applied biological sciences. Psychology ; In Vitro Techniques ; Indomethacin - pharmacology ; Male ; Mas receptor ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide - metabolism ; Peptide Fragments - antagonists & inhibitors ; Peptide Fragments - metabolism ; Peptide Fragments - pharmacology ; Rat aorta ; Rats ; Rats, Sprague-Dawley ; Receptors, Angiotensin - classification ; Receptors, Angiotensin - drug effects ; Receptors, Angiotensin - metabolism ; Vasodilation - drug effects ; Vasodilator effect ; Vertebrates: endocrinology</subject><ispartof>Peptides (New York, N.Y. : 1980), 2007-03, Vol.28 (3), p.702-707</ispartof><rights>2006 Elsevier Inc.</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-1def4e795164be6f2f9e9ff953546b8c8282faf69fbd52fdda5e0a3e9aa180123</citedby><cites>FETCH-LOGICAL-c396t-1def4e795164be6f2f9e9ff953546b8c8282faf69fbd52fdda5e0a3e9aa180123</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0196978106004633$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18517988$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17129638$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Silva, D.M.R.</creatorcontrib><creatorcontrib>Vianna, H.R.</creatorcontrib><creatorcontrib>Cortes, S.F.</creatorcontrib><creatorcontrib>Campagnole-Santos, M.J.</creatorcontrib><creatorcontrib>Santos, R.A.S.</creatorcontrib><creatorcontrib>Lemos, V.S.</creatorcontrib><title>Evidence for a new angiotensin-(1–7) receptor subtype in the aorta of Sprague–Dawley rats</title><title>Peptides (New York, N.Y. : 1980)</title><addtitle>Peptides</addtitle><description>We have recently described, in the mouse aorta, the vasodilator effect of angiotensin-(1–7) (Ang-(1–7)) was mediated by activation of the Mas Ang-(1–7) receptor and that A-779 and D-Pro
7-Ang-(1–7) act as Mas receptor antagonists. In this work we show pharmacological evidence for the existence of a different Ang-(1–7) receptor subtype mediating the vasodilator effect of Ang-(1–7) in the aorta from Sprague–Dawley (SD) rats. Ang-(1–7) induced an endothelium-dependent vasodilator effect in aortic rings from SD rats which was inhibited by removal of the endothelium and by
l-NAME (100
μM) but not by indomethacin (10
μM). The Ang-(1–7) receptor antagonist D-Pro
7-Ang-(1–7) (0.1
μM) abolished the vasodilator effect of the peptide. However, the other specific Ang-(1–7) receptor antagonist, A-779 in concentrations up to 10
μM, did not affect vasodilation induced by Ang-(1–7). The Ang II AT
1 and AT
2 receptors antagonists CV11974 (0.01
μM) and PD123319 (1
μM), respectively, the bradykinin B
2 receptor antagonist HOE 140 (1
μM) and the inhibitor of ACE captopril (10
μM) did not change the effect of Ang-(1–7). Our results show that in the aorta of SD rats, the vasodilator effect of Ang-(1–7) is dependent on endothelium-derived nitric oxide. This effect is mediated by the activation of Ang-(1–7) receptors sensitive to D-Pro
7-Ang-(1–7), but not to A-779, which suggests the existence of a different Ang-(1–7) receptor subtype.</description><subject>Ang-(1–7)</subject><subject>Angiotensin I - antagonists & inhibitors</subject><subject>Angiotensin I - metabolism</subject><subject>Angiotensin I - pharmacology</subject><subject>Angiotensin II - analogs & derivatives</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Aorta, Thoracic - metabolism</subject><subject>Aorta, Thoracic - physiology</subject><subject>Biological and medical sciences</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>In Vitro Techniques</subject><subject>Indomethacin - pharmacology</subject><subject>Male</subject><subject>Mas receptor</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide - metabolism</subject><subject>Peptide Fragments - antagonists & inhibitors</subject><subject>Peptide Fragments - metabolism</subject><subject>Peptide Fragments - pharmacology</subject><subject>Rat aorta</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Angiotensin - classification</subject><subject>Receptors, Angiotensin - drug effects</subject><subject>Receptors, Angiotensin - metabolism</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilator effect</subject><subject>Vertebrates: endocrinology</subject><issn>0196-9781</issn><issn>1873-5169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctu1DAUhi1URKcDrzDyhoouMti5OPYO1JaLVKkLYImsE-d48CiTBNuZana8Q9-wT4KjGdQlqyP9-s5F3yFkxdmaMy7eb9cjjtG1GNY5YyKFa8bqF2TBZV1kFRfqjCwYVyJTteTn5CKELWOsLJV8Rc55zXMlCrkgP2_3aUhvkNrBU6A9PlDoN26I2AfXZ-_405_H-op6NGlfQsLUxMOI1PU0_kIKg49AB0u_jR42Eyb6Bh46PFAPMbwmLy10Ad-c6pL8-HT7_fpLdnf_-ev1x7vMFErEjLdoS6xVOrtsUNjcKlTWqqqoStFII3OZW7BC2aatctu2UCGDAhUAl4znxZJcHueOfvg9YYh654LBroMehyloIZWqy2RmScQRNH4IwaPVo3c78AfNmZ7F6q3-J1bPYuc8iU2Nq9OGqdlh-9x2MpmAtycAgoHOeuiNC8-crHit5Mx9OHKYfOwdeh2Mmx_QuuQ46nZw_7vlL4QfnL8</recordid><startdate>20070301</startdate><enddate>20070301</enddate><creator>Silva, D.M.R.</creator><creator>Vianna, H.R.</creator><creator>Cortes, S.F.</creator><creator>Campagnole-Santos, M.J.</creator><creator>Santos, R.A.S.</creator><creator>Lemos, V.S.</creator><general>Elsevier Inc</general><general>Elsevier Science</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>20070301</creationdate><title>Evidence for a new angiotensin-(1–7) receptor subtype in the aorta of Sprague–Dawley rats</title><author>Silva, D.M.R. ; Vianna, H.R. ; Cortes, S.F. ; Campagnole-Santos, M.J. ; Santos, R.A.S. ; Lemos, V.S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-1def4e795164be6f2f9e9ff953546b8c8282faf69fbd52fdda5e0a3e9aa180123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Ang-(1–7)</topic><topic>Angiotensin I - antagonists & inhibitors</topic><topic>Angiotensin I - metabolism</topic><topic>Angiotensin I - pharmacology</topic><topic>Angiotensin II - analogs & derivatives</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Aorta, Thoracic - drug effects</topic><topic>Aorta, Thoracic - metabolism</topic><topic>Aorta, Thoracic - physiology</topic><topic>Biological and medical sciences</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>In Vitro Techniques</topic><topic>Indomethacin - pharmacology</topic><topic>Male</topic><topic>Mas receptor</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide - metabolism</topic><topic>Peptide Fragments - antagonists & inhibitors</topic><topic>Peptide Fragments - metabolism</topic><topic>Peptide Fragments - pharmacology</topic><topic>Rat aorta</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Angiotensin - classification</topic><topic>Receptors, Angiotensin - drug effects</topic><topic>Receptors, Angiotensin - metabolism</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilator effect</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Silva, D.M.R.</creatorcontrib><creatorcontrib>Vianna, H.R.</creatorcontrib><creatorcontrib>Cortes, S.F.</creatorcontrib><creatorcontrib>Campagnole-Santos, M.J.</creatorcontrib><creatorcontrib>Santos, R.A.S.</creatorcontrib><creatorcontrib>Lemos, V.S.</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>Peptides (New York, N.Y. : 1980)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Silva, D.M.R.</au><au>Vianna, H.R.</au><au>Cortes, S.F.</au><au>Campagnole-Santos, M.J.</au><au>Santos, R.A.S.</au><au>Lemos, V.S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence for a new angiotensin-(1–7) receptor subtype in the aorta of Sprague–Dawley rats</atitle><jtitle>Peptides (New York, N.Y. : 1980)</jtitle><addtitle>Peptides</addtitle><date>2007-03-01</date><risdate>2007</risdate><volume>28</volume><issue>3</issue><spage>702</spage><epage>707</epage><pages>702-707</pages><issn>0196-9781</issn><eissn>1873-5169</eissn><coden>PPTDD5</coden><abstract>We have recently described, in the mouse aorta, the vasodilator effect of angiotensin-(1–7) (Ang-(1–7)) was mediated by activation of the Mas Ang-(1–7) receptor and that A-779 and D-Pro
7-Ang-(1–7) act as Mas receptor antagonists. In this work we show pharmacological evidence for the existence of a different Ang-(1–7) receptor subtype mediating the vasodilator effect of Ang-(1–7) in the aorta from Sprague–Dawley (SD) rats. Ang-(1–7) induced an endothelium-dependent vasodilator effect in aortic rings from SD rats which was inhibited by removal of the endothelium and by
l-NAME (100
μM) but not by indomethacin (10
μM). The Ang-(1–7) receptor antagonist D-Pro
7-Ang-(1–7) (0.1
μM) abolished the vasodilator effect of the peptide. However, the other specific Ang-(1–7) receptor antagonist, A-779 in concentrations up to 10
μM, did not affect vasodilation induced by Ang-(1–7). The Ang II AT
1 and AT
2 receptors antagonists CV11974 (0.01
μM) and PD123319 (1
μM), respectively, the bradykinin B
2 receptor antagonist HOE 140 (1
μM) and the inhibitor of ACE captopril (10
μM) did not change the effect of Ang-(1–7). Our results show that in the aorta of SD rats, the vasodilator effect of Ang-(1–7) is dependent on endothelium-derived nitric oxide. This effect is mediated by the activation of Ang-(1–7) receptors sensitive to D-Pro
7-Ang-(1–7), but not to A-779, which suggests the existence of a different Ang-(1–7) receptor subtype.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>17129638</pmid><doi>10.1016/j.peptides.2006.10.007</doi><tpages>6</tpages></addata></record> |
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source | MEDLINE; Elsevier ScienceDirect Journals |
subjects | Ang-(1–7) Angiotensin I - antagonists & inhibitors Angiotensin I - metabolism Angiotensin I - pharmacology Angiotensin II - analogs & derivatives Angiotensin II - pharmacology Animals Aorta, Thoracic - drug effects Aorta, Thoracic - metabolism Aorta, Thoracic - physiology Biological and medical sciences Fundamental and applied biological sciences. Psychology In Vitro Techniques Indomethacin - pharmacology Male Mas receptor NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - metabolism Peptide Fragments - antagonists & inhibitors Peptide Fragments - metabolism Peptide Fragments - pharmacology Rat aorta Rats Rats, Sprague-Dawley Receptors, Angiotensin - classification Receptors, Angiotensin - drug effects Receptors, Angiotensin - metabolism Vasodilation - drug effects Vasodilator effect Vertebrates: endocrinology |
title | Evidence for a new angiotensin-(1–7) receptor subtype in the aorta of Sprague–Dawley rats |
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