Subcellular and molecular mechanisms of the effects of cardiac glycosides and angiotensin-converting enzyme inhibitors on contractile function and energy conversion in myocardial myofibrils under normal conditions and during acute cardiac insufficiency
Experiments on skinned and hybrid myocardial fibers isolated from normal dogs and animals subjected to 120-min occlusion of the anterior interventricular branch of the coronary artery showed that in contrast to cardiac glycosides, angiotensin-converting enzyme inhibitors suppress contractile ability...
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Veröffentlicht in: | Bulletin of experimental biology and medicine 2002-01, Vol.133 (1), p.74-80 |
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creator | Sukoyan, G V Karsanov, V N Tatulashvili, D R Gochua, E I Samsonidze, T G Karsanov, N V |
description | Experiments on skinned and hybrid myocardial fibers isolated from normal dogs and animals subjected to 120-min occlusion of the anterior interventricular branch of the coronary artery showed that in contrast to cardiac glycosides, angiotensin-converting enzyme inhibitors suppress contractile ability of myocardial myofibrils in a dose-independent manner within the concentration range of 10(-12)-10(-4)M. This effect is accompanied by a decrease in fiber relaxation rate most pronounced in the presence of captopril. Actin, the major protein of fine filaments is the target for b-acetyldigoxin, K-strophanthin, captopril, enalapril, and trandolapril in myocardial myofibrils. During coronary occlusion, the inhibitors of angiotensin-converting enzyme induce structural and conformational changes in actin that decrease efficiency of contraction. The data obtained cast doubt on advisability of therapeutic use of angiotensin-converting enzyme inhibitors in the therapy of myocardial infarction, especially in its early period. |
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This effect is accompanied by a decrease in fiber relaxation rate most pronounced in the presence of captopril. Actin, the major protein of fine filaments is the target for b-acetyldigoxin, K-strophanthin, captopril, enalapril, and trandolapril in myocardial myofibrils. During coronary occlusion, the inhibitors of angiotensin-converting enzyme induce structural and conformational changes in actin that decrease efficiency of contraction. The data obtained cast doubt on advisability of therapeutic use of angiotensin-converting enzyme inhibitors in the therapy of myocardial infarction, especially in its early period.</description><identifier>ISSN: 0007-4888</identifier><identifier>EISSN: 1573-8221</identifier><identifier>DOI: 10.1023/A:1015168814082</identifier><identifier>PMID: 12170313</identifier><identifier>CODEN: BEXBAN</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Actins - chemistry ; Acute Disease ; Angiotensin-Converting Enzyme Inhibitors - pharmacology ; Animals ; Cardiac Glycosides - antagonists & inhibitors ; Dogs ; Energy Metabolism ; In Vitro Techniques ; Models, Molecular ; Myocardial Contraction - drug effects ; Myocardial Ischemia - metabolism ; Myocardial Ischemia - physiopathology ; Myocardium - metabolism ; Myocardium - ultrastructure ; Myofibrils - drug effects ; Myofibrils - metabolism ; Protein Conformation</subject><ispartof>Bulletin of experimental biology and medicine, 2002-01, Vol.133 (1), p.74-80</ispartof><rights>Copyright (c) 2002 Plenum Publishing Corporation</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c195t-53b619f659af182aa51c9dcf77a6dc9ce43e8cb001f8997fafabc38ad917f003</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12170313$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sukoyan, G V</creatorcontrib><creatorcontrib>Karsanov, V N</creatorcontrib><creatorcontrib>Tatulashvili, D R</creatorcontrib><creatorcontrib>Gochua, E I</creatorcontrib><creatorcontrib>Samsonidze, T G</creatorcontrib><creatorcontrib>Karsanov, N V</creatorcontrib><title>Subcellular and molecular mechanisms of the effects of cardiac glycosides and angiotensin-converting enzyme inhibitors on contractile function and energy conversion in myocardial myofibrils under normal conditions and during acute cardiac insufficiency</title><title>Bulletin of experimental biology and medicine</title><addtitle>Bull Exp Biol Med</addtitle><description>Experiments on skinned and hybrid myocardial fibers isolated from normal dogs and animals subjected to 120-min occlusion of the anterior interventricular branch of the coronary artery showed that in contrast to cardiac glycosides, angiotensin-converting enzyme inhibitors suppress contractile ability of myocardial myofibrils in a dose-independent manner within the concentration range of 10(-12)-10(-4)M. 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subjects | Actins - chemistry Acute Disease Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Cardiac Glycosides - antagonists & inhibitors Dogs Energy Metabolism In Vitro Techniques Models, Molecular Myocardial Contraction - drug effects Myocardial Ischemia - metabolism Myocardial Ischemia - physiopathology Myocardium - metabolism Myocardium - ultrastructure Myofibrils - drug effects Myofibrils - metabolism Protein Conformation |
title | Subcellular and molecular mechanisms of the effects of cardiac glycosides and angiotensin-converting enzyme inhibitors on contractile function and energy conversion in myocardial myofibrils under normal conditions and during acute cardiac insufficiency |
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