Role of endothelin in deterioration of heart failure due to cardiomyopathy in hamsters : Increase in endothelin-1 production in the heart and beneficial effect of endothelin-A receptor antagonist on survival and cardiac function
We previously reported that chronic endothelin (ET) receptor blockade ameliorated the survival rate and cardiac hemodynamics in rats with chronic heart failure (CHF) due to myocardial infarction. However, it remains unclear whether ET-1 is involved in the pathophysiology of cardiomyopathy, which is...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1999-04, Vol.99 (16), p.2171-2176 |
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| creator | YAMAUCHI-KOHNO, R MIYAUCHI, T HOSHINO, T KOBAYASHI, T AIHARA, H SAKAI, S YABANA, H GOTO, K SUGISHITA, Y MURATA, S |
| description | We previously reported that chronic endothelin (ET) receptor blockade ameliorated the survival rate and cardiac hemodynamics in rats with chronic heart failure (CHF) due to myocardial infarction. However, it remains unclear whether ET-1 is involved in the pathophysiology of cardiomyopathy, which is one of the major causes of CHF. Accordingly, we investigated the production of ET-1 in the heart and the effect of chronic ETA receptor blockade on survival rate and cardiac function in the Bio 14.6 hamster, which is an idiopathic model of CHF caused by cardiomyopathy.
We used 52-week-old Bio 14.6 cardiomyopathic hamsters and age-matched F1b normal hamsters. The expression of preproET-1 mRNA and the ET-1 level in the hearts were markedly higher in the cardiomyopathic hamsters than in the normal hamsters. The cardiomyopathic hamsters showed severe CHF, illustrated by lower left ventricular (LV) +dP/dt/Pmax and right ventricular (RV) +dP/dt/Pmax and by higher LV end-diastolic pressure (EDP), RVEDP, and central venous pressure compared with the normal hamsters. Long-term (9 weeks) treatment with an ETA antagonist (TA-0201, 1.3 mg. kg-1. d-1) markedly increased survival of cardiomyopathic hamsters (untreated, 16%; TA-0201-treated, 65.2%; P |
| doi_str_mv | 10.1161/01.CIR.99.16.2171 |
| format | Article |
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We used 52-week-old Bio 14.6 cardiomyopathic hamsters and age-matched F1b normal hamsters. The expression of preproET-1 mRNA and the ET-1 level in the hearts were markedly higher in the cardiomyopathic hamsters than in the normal hamsters. The cardiomyopathic hamsters showed severe CHF, illustrated by lower left ventricular (LV) +dP/dt/Pmax and right ventricular (RV) +dP/dt/Pmax and by higher LV end-diastolic pressure (EDP), RVEDP, and central venous pressure compared with the normal hamsters. Long-term (9 weeks) treatment with an ETA antagonist (TA-0201, 1.3 mg. kg-1. d-1) markedly increased survival of cardiomyopathic hamsters (untreated, 16%; TA-0201-treated, 65.2%; P<0.001). After 6 weeks of treatment, LV +dP/dt/Pmax and RV +dP/dt/Pmax were significantly higher and LVEDP and RVEDP were lower in the TA-0201-treated group than in the untreated group, suggesting that chronic TA-0201 treatment effectively prevented deterioration of cardiac dysfunction.
In the cardiomyopathic hamsters with CHF, the production of ET-1 in the heart was markedly increased, and chronic ETA receptor blockade greatly ameliorated survival and cardiac dysfunction. These results suggest that ET-1 plays an important role in the deterioration of CHF caused by cardiomyopathy, and ETA antagonists may exert therapeutic effects in CHF due to cardiomyopathy.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.99.16.2171</identifier><identifier>PMID: 10217659</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Biological and medical sciences ; Blood Pressure - drug effects ; Cardiology. Vascular system ; Cardiomyopathies - genetics ; Cardiomyopathies - physiopathology ; Cricetinae ; Endothelin Receptor Antagonists ; Endothelin-1 - genetics ; Endothelin-1 - physiology ; Heart ; Heart Failure - drug therapy ; Heart Failure - etiology ; Heart Failure - physiopathology ; Heart Rate - drug effects ; Hemodynamics - drug effects ; Hemodynamics - physiology ; Male ; Medical sciences ; Myocarditis. Cardiomyopathies ; Myocardium - metabolism ; Pyrimidines - pharmacology ; Pyrimidines - therapeutic use ; Rats ; Receptor, Endothelin A ; Sulfonamides - pharmacology ; Sulfonamides - therapeutic use ; Survival Rate ; Ventricular Function, Left - drug effects ; Ventricular Function, Right - drug effects</subject><ispartof>Circulation (New York, N.Y.), 1999-04, Vol.99 (16), p.2171-2176</ispartof><rights>1999 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Apr 27, 1999</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c347t-86203ec8c2ee67a820eba44b7c8476fb6b55cb251a06bb9be7b5b2d0fe6927463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1762755$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10217659$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YAMAUCHI-KOHNO, R</creatorcontrib><creatorcontrib>MIYAUCHI, T</creatorcontrib><creatorcontrib>HOSHINO, T</creatorcontrib><creatorcontrib>KOBAYASHI, T</creatorcontrib><creatorcontrib>AIHARA, H</creatorcontrib><creatorcontrib>SAKAI, S</creatorcontrib><creatorcontrib>YABANA, H</creatorcontrib><creatorcontrib>GOTO, K</creatorcontrib><creatorcontrib>SUGISHITA, Y</creatorcontrib><creatorcontrib>MURATA, S</creatorcontrib><title>Role of endothelin in deterioration of heart failure due to cardiomyopathy in hamsters : Increase in endothelin-1 production in the heart and beneficial effect of endothelin-A receptor antagonist on survival and cardiac function</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>We previously reported that chronic endothelin (ET) receptor blockade ameliorated the survival rate and cardiac hemodynamics in rats with chronic heart failure (CHF) due to myocardial infarction. However, it remains unclear whether ET-1 is involved in the pathophysiology of cardiomyopathy, which is one of the major causes of CHF. Accordingly, we investigated the production of ET-1 in the heart and the effect of chronic ETA receptor blockade on survival rate and cardiac function in the Bio 14.6 hamster, which is an idiopathic model of CHF caused by cardiomyopathy.
We used 52-week-old Bio 14.6 cardiomyopathic hamsters and age-matched F1b normal hamsters. The expression of preproET-1 mRNA and the ET-1 level in the hearts were markedly higher in the cardiomyopathic hamsters than in the normal hamsters. The cardiomyopathic hamsters showed severe CHF, illustrated by lower left ventricular (LV) +dP/dt/Pmax and right ventricular (RV) +dP/dt/Pmax and by higher LV end-diastolic pressure (EDP), RVEDP, and central venous pressure compared with the normal hamsters. Long-term (9 weeks) treatment with an ETA antagonist (TA-0201, 1.3 mg. kg-1. d-1) markedly increased survival of cardiomyopathic hamsters (untreated, 16%; TA-0201-treated, 65.2%; P<0.001). After 6 weeks of treatment, LV +dP/dt/Pmax and RV +dP/dt/Pmax were significantly higher and LVEDP and RVEDP were lower in the TA-0201-treated group than in the untreated group, suggesting that chronic TA-0201 treatment effectively prevented deterioration of cardiac dysfunction.
In the cardiomyopathic hamsters with CHF, the production of ET-1 in the heart was markedly increased, and chronic ETA receptor blockade greatly ameliorated survival and cardiac dysfunction. These results suggest that ET-1 plays an important role in the deterioration of CHF caused by cardiomyopathy, and ETA antagonists may exert therapeutic effects in CHF due to cardiomyopathy.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Cardiology. Vascular system</subject><subject>Cardiomyopathies - genetics</subject><subject>Cardiomyopathies - physiopathology</subject><subject>Cricetinae</subject><subject>Endothelin Receptor Antagonists</subject><subject>Endothelin-1 - genetics</subject><subject>Endothelin-1 - physiology</subject><subject>Heart</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - etiology</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Rate - drug effects</subject><subject>Hemodynamics - drug effects</subject><subject>Hemodynamics - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>Myocardium - metabolism</subject><subject>Pyrimidines - pharmacology</subject><subject>Pyrimidines - therapeutic use</subject><subject>Rats</subject><subject>Receptor, Endothelin A</subject><subject>Sulfonamides - pharmacology</subject><subject>Sulfonamides - therapeutic use</subject><subject>Survival Rate</subject><subject>Ventricular Function, Left - drug effects</subject><subject>Ventricular Function, Right - drug effects</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkd-K1DAUxoso7rj6AN5IEPGuNUnbpPFuGfwzsCAseh2S9MTJ0iZjki7M-_ogpjMDq0Ig5Jzf950Tvqp6TXBDCCMfMGm2u7tGiIawhhJOnlQb0tOu7vpWPK02GGNR85bSq-pFSvflyVreP6-uCC4068Wm-n0XJkDBIvBjyHuYnEfljJAhuhBVdsGv7T2omJFVbloioHEBlAMyKo4uzMdwUHl_XHV7NaeiTOgj2nkTQSVYy4_mNUGHGMbFnIxLq5Qv5sqPSIMH64xTEwJrweR_V6tvUAQDhxxiwbP6GbxLhfEoLfHBPRTZ6nLaSxlkF3-a87J6ZtWU4NXlvq5-fP70ffu1vv32Zbe9ua1N2_FcD4ziFsxgKADjaqAYtOo6zc3QcWY1031vNO2JwkxroYHrXtMRW2CC8o6119X7s2_54q8FUpazSwamSXkIS5JMcNK1dAXf_gfehyX6spukZLXi7VAgcoZMDClFsPIQ3aziURIs1_wlJrLkL4WQhMk1_6J5czFe9AzjX4pz4AV4dwFUMmqyUXnj0iPHGeV93_4Bk5G9kg</recordid><startdate>19990427</startdate><enddate>19990427</enddate><creator>YAMAUCHI-KOHNO, R</creator><creator>MIYAUCHI, T</creator><creator>HOSHINO, T</creator><creator>KOBAYASHI, T</creator><creator>AIHARA, H</creator><creator>SAKAI, S</creator><creator>YABANA, H</creator><creator>GOTO, K</creator><creator>SUGISHITA, Y</creator><creator>MURATA, S</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>19990427</creationdate><title>Role of endothelin in deterioration of heart failure due to cardiomyopathy in hamsters : Increase in endothelin-1 production in the heart and beneficial effect of endothelin-A receptor antagonist on survival and cardiac function</title><author>YAMAUCHI-KOHNO, R ; MIYAUCHI, T ; HOSHINO, T ; KOBAYASHI, T ; AIHARA, H ; SAKAI, S ; YABANA, H ; GOTO, K ; SUGISHITA, Y ; MURATA, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c347t-86203ec8c2ee67a820eba44b7c8476fb6b55cb251a06bb9be7b5b2d0fe6927463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiology. Vascular system</topic><topic>Cardiomyopathies - genetics</topic><topic>Cardiomyopathies - physiopathology</topic><topic>Cricetinae</topic><topic>Endothelin Receptor Antagonists</topic><topic>Endothelin-1 - genetics</topic><topic>Endothelin-1 - physiology</topic><topic>Heart</topic><topic>Heart Failure - drug therapy</topic><topic>Heart Failure - etiology</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Rate - drug effects</topic><topic>Hemodynamics - drug effects</topic><topic>Hemodynamics - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>Myocardium - metabolism</topic><topic>Pyrimidines - pharmacology</topic><topic>Pyrimidines - therapeutic use</topic><topic>Rats</topic><topic>Receptor, Endothelin A</topic><topic>Sulfonamides - pharmacology</topic><topic>Sulfonamides - therapeutic use</topic><topic>Survival Rate</topic><topic>Ventricular Function, Left - drug effects</topic><topic>Ventricular Function, Right - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YAMAUCHI-KOHNO, R</creatorcontrib><creatorcontrib>MIYAUCHI, T</creatorcontrib><creatorcontrib>HOSHINO, T</creatorcontrib><creatorcontrib>KOBAYASHI, T</creatorcontrib><creatorcontrib>AIHARA, H</creatorcontrib><creatorcontrib>SAKAI, S</creatorcontrib><creatorcontrib>YABANA, H</creatorcontrib><creatorcontrib>GOTO, K</creatorcontrib><creatorcontrib>SUGISHITA, Y</creatorcontrib><creatorcontrib>MURATA, 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>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>YAMAUCHI-KOHNO, R</au><au>MIYAUCHI, T</au><au>HOSHINO, T</au><au>KOBAYASHI, T</au><au>AIHARA, H</au><au>SAKAI, S</au><au>YABANA, H</au><au>GOTO, K</au><au>SUGISHITA, Y</au><au>MURATA, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of endothelin in deterioration of heart failure due to cardiomyopathy in hamsters : Increase in endothelin-1 production in the heart and beneficial effect of endothelin-A receptor antagonist on survival and cardiac function</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1999-04-27</date><risdate>1999</risdate><volume>99</volume><issue>16</issue><spage>2171</spage><epage>2176</epage><pages>2171-2176</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>We previously reported that chronic endothelin (ET) receptor blockade ameliorated the survival rate and cardiac hemodynamics in rats with chronic heart failure (CHF) due to myocardial infarction. However, it remains unclear whether ET-1 is involved in the pathophysiology of cardiomyopathy, which is one of the major causes of CHF. Accordingly, we investigated the production of ET-1 in the heart and the effect of chronic ETA receptor blockade on survival rate and cardiac function in the Bio 14.6 hamster, which is an idiopathic model of CHF caused by cardiomyopathy.
We used 52-week-old Bio 14.6 cardiomyopathic hamsters and age-matched F1b normal hamsters. The expression of preproET-1 mRNA and the ET-1 level in the hearts were markedly higher in the cardiomyopathic hamsters than in the normal hamsters. The cardiomyopathic hamsters showed severe CHF, illustrated by lower left ventricular (LV) +dP/dt/Pmax and right ventricular (RV) +dP/dt/Pmax and by higher LV end-diastolic pressure (EDP), RVEDP, and central venous pressure compared with the normal hamsters. Long-term (9 weeks) treatment with an ETA antagonist (TA-0201, 1.3 mg. kg-1. d-1) markedly increased survival of cardiomyopathic hamsters (untreated, 16%; TA-0201-treated, 65.2%; P<0.001). After 6 weeks of treatment, LV +dP/dt/Pmax and RV +dP/dt/Pmax were significantly higher and LVEDP and RVEDP were lower in the TA-0201-treated group than in the untreated group, suggesting that chronic TA-0201 treatment effectively prevented deterioration of cardiac dysfunction.
In the cardiomyopathic hamsters with CHF, the production of ET-1 in the heart was markedly increased, and chronic ETA receptor blockade greatly ameliorated survival and cardiac dysfunction. These results suggest that ET-1 plays an important role in the deterioration of CHF caused by cardiomyopathy, and ETA antagonists may exert therapeutic effects in CHF due to cardiomyopathy.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>10217659</pmid><doi>10.1161/01.CIR.99.16.2171</doi><tpages>6</tpages></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 1999-04, Vol.99 (16), p.2171-2176 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete |
| subjects | Animals Biological and medical sciences Blood Pressure - drug effects Cardiology. Vascular system Cardiomyopathies - genetics Cardiomyopathies - physiopathology Cricetinae Endothelin Receptor Antagonists Endothelin-1 - genetics Endothelin-1 - physiology Heart Heart Failure - drug therapy Heart Failure - etiology Heart Failure - physiopathology Heart Rate - drug effects Hemodynamics - drug effects Hemodynamics - physiology Male Medical sciences Myocarditis. Cardiomyopathies Myocardium - metabolism Pyrimidines - pharmacology Pyrimidines - therapeutic use Rats Receptor, Endothelin A Sulfonamides - pharmacology Sulfonamides - therapeutic use Survival Rate Ventricular Function, Left - drug effects Ventricular Function, Right - drug effects |
| title | Role of endothelin in deterioration of heart failure due to cardiomyopathy in hamsters : Increase in endothelin-1 production in the heart and beneficial effect of endothelin-A receptor antagonist on survival and cardiac function |
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