title: Alterations in sarcoplasmic reticulum and angiotensin II type 1 receptor gene expression after myocardial infarction in rats.
abstract: The purpose of this study was to investigate the function of sarcoplasmic reticulum (SR) and the role of angiotensin II type 1 receptor (AT1) in ventricular remodeling in non-infarcted areas after myocardial infarction (MI). MI was produced in anesthetized Sprague-Dawley rats (10-12-weeks old) by ligation of the left anterior descending coronary artery. Four weeks after MI, hemodynamic measurements were performed. SR Ca2+-ATPase activity and mRNA (SERCA2a) and AT1 mRNA (AT1a, AT1b) were analyzed. Left ventricular end-diastolic pressure was higher and left ventricular dp/dt was significantly lower in the MI group. In non-infarcted areas in the MI group, myocardial transverse diameter was significantly greater and both Ca2+-ATPase activity in the SR and SERCA2a level decreased. The AT1a level was higher in non-infarcted areas than in controls, whereas the AT1b mRNA expression level was unchanged. These results suggest that, in the ventricular remodeling after MI, alterations in SR protein and its mRNA in non-infarcted myocardium help initiate heart failure and that Ca overload caused by the up-regulation of AT1a mRNA is an important cause of alteration in SR function.
authors.affiliation: Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Iijima
authors.forename: E
authors.initials: E
authors.lastname: Geshi
authors.forename: A
authors.initials: A
authors.lastname: Nomizo
authors.forename: Y
authors.initials: Y
authors.lastname: Arata
authors.forename: T
authors.initials: T
authors.lastname: Katagiri
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000096:biosynthesis / Q000235:genetics; D005355:Fibrosis; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D006352:Heart Ventricles / Q000473:pathology; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D007527:Isoenzymes / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D009124:Muscle Proteins / Q000096:biosynthesis / Q000235:genetics; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000096:biosynthesis* / Q000235:genetics; D012519:Sarcoplasmic Reticulum / Q000502:physiology*; D018487:Ventricular Dysfunction, Left / Q000378:metabolism / Q000473:pathology
chemical_list: D007527:Isoenzymes; D009124:Muscle Proteins; D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D000252:Calcium-Transporting ATPases; D002118:Calcium