title: Regional expression of endothelin-1, ANP, IGF-1, and LV wall stress in the infarcted rat heart.
abstract: We hypothesized that myocardial infarction induces regional and temporal differences in endothelin-1 (ET-1), atrial natriuretic peptide (ANP), and insulin-like growth factor-1 (IGF-1) gene expression that correlate with left ventricular (LV) wall stress. Echocardiography and LV pressure measurements were performed in coronary artery-ligated or sham-operated rats. Gene expression was measured by competitive RT-PCR in the infarct, border zone, and remote area and in regionally isolated cardiomyocytes. ET-1 and IGF-1 expression was highest in the infarcted myocardium, whereas ANP expression was highest in noninfarcted myocardium. For all genes, remote area expression was highest after 7 days. At 42 days, ANP maintained maximum expression, ET-1 decreased to 50% of peak levels, and IGF-1 was normalized. Cardiomyocyte expression followed the same pattern as in the myocardium except for a markedly lower IGF-1 expression. Diastolic wall stress was the best hemodynamic variable to predict ET-1 and ANP expression in the remote area. We conclude that ET-1, ANP, and IGF-1 are expressed in different patterns in the infarcted heart in relation to time, functional regions, cellular distribution, and mechanical load.
authors.affiliation: Department of Physiology and Biomedical Engineering, Norwegian University of Science and Technology, N-7489 Trondheim, Norway.
authors.forename: J P
authors.initials: JP
authors.lastname: Loennechen
authors.forename: A
authors.initials: A
authors.lastname: Støylen
authors.forename: V
authors.initials: V
authors.lastname: Beisvag
authors.forename: U
authors.initials: U
authors.lastname: Wisløff
authors.forename: O
authors.initials: O
authors.lastname: Ellingsen
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000096:biosynthesis* / Q000235:genetics; D001794:Blood Pressure; D003971:Diastole; D004195:Disease Models, Animal; D019332:Endothelin-1 / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D015870:Gene Expression; D006352:Heart Ventricles / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics; D007334:Insulin-Like Growth Factor I / Q000096:biosynthesis* / Q000235:genetics; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013314:Stress, Mechanical; D016277:Ventricular Function, Left
chemical_list: D019332:Endothelin-1; D012333:RNA, Messenger; D007334:Insulin-Like Growth Factor I; D009320:Atrial Natriuretic Factor