Angiotensin-(1-7) attenuates the development of heart failure after myocardial infarction in rats
The renin-angiotensin system (RAS) is a key player in the progression of heart failure. Angiotensin-(1-7) is thought to modulate the activity of the RAS. Furthermore, this peptide may play a part in the beneficial effects of angiotensin-converting enzyme inhibitors in cardiovascular disease. We asse...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2002-04, Vol.105 (13), p.1548-1550 |
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| container_title | Circulation (New York, N.Y.) |
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| creator | LOOT, Annemarieke E ROKS, Anton J. M HENNING, Robert H TIO, René A SUURMEIJER, Albert J. H BOOMSMA, Frans VAN GILST, Wiek H |
| description | The renin-angiotensin system (RAS) is a key player in the progression of heart failure. Angiotensin-(1-7) is thought to modulate the activity of the RAS. Furthermore, this peptide may play a part in the beneficial effects of angiotensin-converting enzyme inhibitors in cardiovascular disease. We assessed the effects of angiotensin-(1-7) on the progression of heart failure.
Male Sprague-Dawley rats underwent either coronary ligation or sham surgery. Two weeks after induction of myocardial infarction, intravenous infusion of angiotensin-(1-7) (24 microg/kg per hour) or saline was started by minipump. After 8 weeks of treatment, hemodynamic parameters were measured, endothelial function was assessed in isolated aortic rings, and plasma angiotensin-(1-7) levels were determined. Myocardial infarction resulted in a significant deterioration of left ventricular systolic and diastolic pressure, dP/dt, and coronary flow. Raising plasma levels 40-fold, angiotensin-(1-7) infusion attenuated this impairment to a nonsignificant level, markedly illustrated by a 40% reduction in left ventricular end-diastolic pressure. Furthermore, angiotensin-(1-7) completely preserved aortic endothelial function, whereas endothelium-dependent relaxation in aortas of saline-treated infarcted rats was significantly decreased.
Angiotensin-(1-7) preserved cardiac function, coronary perfusion, and aortic endothelial function in a rat model for heart failure. |
| doi_str_mv | 10.1161/01.cir.0000013847.07035.b9 |
| format | Article |
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Male Sprague-Dawley rats underwent either coronary ligation or sham surgery. Two weeks after induction of myocardial infarction, intravenous infusion of angiotensin-(1-7) (24 microg/kg per hour) or saline was started by minipump. After 8 weeks of treatment, hemodynamic parameters were measured, endothelial function was assessed in isolated aortic rings, and plasma angiotensin-(1-7) levels were determined. Myocardial infarction resulted in a significant deterioration of left ventricular systolic and diastolic pressure, dP/dt, and coronary flow. Raising plasma levels 40-fold, angiotensin-(1-7) infusion attenuated this impairment to a nonsignificant level, markedly illustrated by a 40% reduction in left ventricular end-diastolic pressure. Furthermore, angiotensin-(1-7) completely preserved aortic endothelial function, whereas endothelium-dependent relaxation in aortas of saline-treated infarcted rats was significantly decreased.
Angiotensin-(1-7) preserved cardiac function, coronary perfusion, and aortic endothelial function in a rat model for heart failure.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.0000013847.07035.b9</identifier><identifier>PMID: 11927520</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Angiotensin I - administration & dosage ; Angiotensin I - therapeutic use ; Animals ; Aorta - drug effects ; Aorta - physiopathology ; Biological and medical sciences ; Cardiology. Vascular system ; Coronary Circulation - drug effects ; Culture Techniques ; Endothelium, Vascular - physiopathology ; Heart ; Heart Failure - etiology ; Heart Failure - physiopathology ; Heart Failure - prevention & control ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Hemodynamics ; Infusions, Intravenous ; Male ; Medical sciences ; Myocardial Infarction - complications ; Peptide Fragments - administration & dosage ; Peptide Fragments - therapeutic use ; Rats ; Rats, Sprague-Dawley ; Vasodilation - drug effects</subject><ispartof>Circulation (New York, N.Y.), 2002-04, Vol.105 (13), p.1548-1550</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Apr 2, 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c590t-e53e61ed9b2b185e5b843d94043608650e6d48bf827f3985165725b90a2825523</citedby><cites>FETCH-LOGICAL-c590t-e53e61ed9b2b185e5b843d94043608650e6d48bf827f3985165725b90a2825523</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13603378$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11927520$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LOOT, Annemarieke E</creatorcontrib><creatorcontrib>ROKS, Anton J. M</creatorcontrib><creatorcontrib>HENNING, Robert H</creatorcontrib><creatorcontrib>TIO, René A</creatorcontrib><creatorcontrib>SUURMEIJER, Albert J. H</creatorcontrib><creatorcontrib>BOOMSMA, Frans</creatorcontrib><creatorcontrib>VAN GILST, Wiek H</creatorcontrib><title>Angiotensin-(1-7) attenuates the development of heart failure after myocardial infarction in rats</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>The renin-angiotensin system (RAS) is a key player in the progression of heart failure. Angiotensin-(1-7) is thought to modulate the activity of the RAS. Furthermore, this peptide may play a part in the beneficial effects of angiotensin-converting enzyme inhibitors in cardiovascular disease. We assessed the effects of angiotensin-(1-7) on the progression of heart failure.
Male Sprague-Dawley rats underwent either coronary ligation or sham surgery. Two weeks after induction of myocardial infarction, intravenous infusion of angiotensin-(1-7) (24 microg/kg per hour) or saline was started by minipump. After 8 weeks of treatment, hemodynamic parameters were measured, endothelial function was assessed in isolated aortic rings, and plasma angiotensin-(1-7) levels were determined. Myocardial infarction resulted in a significant deterioration of left ventricular systolic and diastolic pressure, dP/dt, and coronary flow. Raising plasma levels 40-fold, angiotensin-(1-7) infusion attenuated this impairment to a nonsignificant level, markedly illustrated by a 40% reduction in left ventricular end-diastolic pressure. Furthermore, angiotensin-(1-7) completely preserved aortic endothelial function, whereas endothelium-dependent relaxation in aortas of saline-treated infarcted rats was significantly decreased.
Angiotensin-(1-7) preserved cardiac function, coronary perfusion, and aortic endothelial function in a rat model for heart failure.</description><subject>Angiotensin I - administration & dosage</subject><subject>Angiotensin I - therapeutic use</subject><subject>Animals</subject><subject>Aorta - drug effects</subject><subject>Aorta - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary Circulation - drug effects</subject><subject>Culture Techniques</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Heart</subject><subject>Heart Failure - etiology</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Failure - prevention & control</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Hemodynamics</subject><subject>Infusions, Intravenous</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Infarction - complications</subject><subject>Peptide Fragments - administration & dosage</subject><subject>Peptide Fragments - therapeutic use</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Vasodilation - drug effects</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkVtrFTEQx4Mo9lj9ChIKij7smsvm1rd68FIoCKLPIbs7sSm7yTHJCv32pvbAAedlZpjfTDLzR-iCkp5SST8Q2k8h9-TBKNeD6okiXPSjeYJ2VLChGwQ3T9Gu1U2nOGNn6EUpdy2VXInn6IxSw5RgZIfcVfwVUoVYQuze0U69x662dHMVCq63gGf4A0s6rBArTh7fgssVexeWLQN2vkLG632aXJ6DW3CI3uWphhRbiLOr5SV65t1S4NXRn6Ofnz_92H_tbr59ud5f3XSTMKR2IDhICrMZ2Ui1ADHqgc9mIAOXREtBQM6DHr1mynOjBZVCMTEa4phmQjB-jt4-zj3k9HuDUu0aygTL4iKkrVhFZZtlhgZe_AfepS3H9jfLKFNScskbdPkITTmVksHbQw6ry_eWEvuggiXU7q-_25MK9p8K9qNpza-PL2zjCvOp9Xj2Brw5Aq5MbvHZxSmUE9dW5lxp_hdC_I7U</recordid><startdate>20020402</startdate><enddate>20020402</enddate><creator>LOOT, Annemarieke E</creator><creator>ROKS, Anton J. M</creator><creator>HENNING, Robert H</creator><creator>TIO, René A</creator><creator>SUURMEIJER, Albert J. H</creator><creator>BOOMSMA, Frans</creator><creator>VAN GILST, Wiek H</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20020402</creationdate><title>Angiotensin-(1-7) attenuates the development of heart failure after myocardial infarction in rats</title><author>LOOT, Annemarieke E ; ROKS, Anton J. M ; HENNING, Robert H ; TIO, René A ; SUURMEIJER, Albert J. H ; BOOMSMA, Frans ; VAN GILST, Wiek H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c590t-e53e61ed9b2b185e5b843d94043608650e6d48bf827f3985165725b90a2825523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Angiotensin I - administration & dosage</topic><topic>Angiotensin I - therapeutic use</topic><topic>Animals</topic><topic>Aorta - drug effects</topic><topic>Aorta - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary Circulation - drug effects</topic><topic>Culture Techniques</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Heart</topic><topic>Heart Failure - etiology</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Failure - prevention & control</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Hemodynamics</topic><topic>Infusions, Intravenous</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Infarction - complications</topic><topic>Peptide Fragments - administration & dosage</topic><topic>Peptide Fragments - therapeutic use</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Vasodilation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LOOT, Annemarieke E</creatorcontrib><creatorcontrib>ROKS, Anton J. M</creatorcontrib><creatorcontrib>HENNING, Robert H</creatorcontrib><creatorcontrib>TIO, René A</creatorcontrib><creatorcontrib>SUURMEIJER, Albert J. H</creatorcontrib><creatorcontrib>BOOMSMA, Frans</creatorcontrib><creatorcontrib>VAN GILST, Wiek H</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LOOT, Annemarieke E</au><au>ROKS, Anton J. M</au><au>HENNING, Robert H</au><au>TIO, René A</au><au>SUURMEIJER, Albert J. H</au><au>BOOMSMA, Frans</au><au>VAN GILST, Wiek H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin-(1-7) attenuates the development of heart failure after myocardial infarction in rats</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2002-04-02</date><risdate>2002</risdate><volume>105</volume><issue>13</issue><spage>1548</spage><epage>1550</epage><pages>1548-1550</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>The renin-angiotensin system (RAS) is a key player in the progression of heart failure. Angiotensin-(1-7) is thought to modulate the activity of the RAS. Furthermore, this peptide may play a part in the beneficial effects of angiotensin-converting enzyme inhibitors in cardiovascular disease. We assessed the effects of angiotensin-(1-7) on the progression of heart failure.
Male Sprague-Dawley rats underwent either coronary ligation or sham surgery. Two weeks after induction of myocardial infarction, intravenous infusion of angiotensin-(1-7) (24 microg/kg per hour) or saline was started by minipump. After 8 weeks of treatment, hemodynamic parameters were measured, endothelial function was assessed in isolated aortic rings, and plasma angiotensin-(1-7) levels were determined. Myocardial infarction resulted in a significant deterioration of left ventricular systolic and diastolic pressure, dP/dt, and coronary flow. Raising plasma levels 40-fold, angiotensin-(1-7) infusion attenuated this impairment to a nonsignificant level, markedly illustrated by a 40% reduction in left ventricular end-diastolic pressure. Furthermore, angiotensin-(1-7) completely preserved aortic endothelial function, whereas endothelium-dependent relaxation in aortas of saline-treated infarcted rats was significantly decreased.
Angiotensin-(1-7) preserved cardiac function, coronary perfusion, and aortic endothelial function in a rat model for heart failure.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>11927520</pmid><doi>10.1161/01.cir.0000013847.07035.b9</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 2002-04, Vol.105 (13), p.1548-1550 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Angiotensin I - administration & dosage Angiotensin I - therapeutic use Animals Aorta - drug effects Aorta - physiopathology Biological and medical sciences Cardiology. Vascular system Coronary Circulation - drug effects Culture Techniques Endothelium, Vascular - physiopathology Heart Heart Failure - etiology Heart Failure - physiopathology Heart Failure - prevention & control Heart failure, cardiogenic pulmonary edema, cardiac enlargement Hemodynamics Infusions, Intravenous Male Medical sciences Myocardial Infarction - complications Peptide Fragments - administration & dosage Peptide Fragments - therapeutic use Rats Rats, Sprague-Dawley Vasodilation - drug effects |
| title | Angiotensin-(1-7) attenuates the development of heart failure after myocardial infarction in rats |
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