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pubmed-article:7856282pubmed:abstractTextIt is known that angiotensin converting enzyme (ACE) inhibitors not only prevent the formation of angiotensin II, but also potentiate the activity of bradykinin. We investigated the effects of the ACE-inhibitor ramipril in two models of cardiac ischemia. In anesthetized dogs with a coronary occlusion of 6-h duration, both ramiprilat and bradykinin significantly reduced infarct-size. This effect was prevented by the co-administration of the bradykinin antagonist HOE 140. In rats with a coronary occlusion of 6-weeks duration, ramipril administration significantly reduced infarct-size and prevented the development of left ventricular hypertrophy. Thus, ramipril showed a cardioprotective activity in models of acute as well as of chronic myocardial ischemia. These effects are probably mediated by the potentiation of bradykinin.lld:pubmed
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pubmed-article:7856282pubmed:volume83 Suppl 4lld:pubmed
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pubmed-article:7856282pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:7856282pubmed:year1994lld:pubmed
pubmed-article:7856282pubmed:articleTitle[Reduction of infarct size and remodeling after ramipril].lld:pubmed
pubmed-article:7856282pubmed:affiliationCassella AG, SGE Herz-Kreislauf Therapeutika, Frankfurt/Main.lld:pubmed
pubmed-article:7856282pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7856282pubmed:publicationTypeEnglish Abstractlld:pubmed