title: Upregulation of angiotensin AT1a receptors mRNA in the heart and renal medulla after myocardial infarction in rats.
abstract: The myocardial infarct causes prolonged activation of the renin-angiotensin system and profoundly influences cardiac performance and renal excretory capabilities. The aim of the present study was to determine whether the myocardial infarct is also associated with an altered expression of AT1a receptors (AT1aR) mRNA in the heart and the kidney. To this end male Sprague-Dawley rats were subjected either to the left coronary artery ligation or to the sham surgery. Four weeks after the surgery the animals were sacrificed. In 11 infarcted and 10 sham-operated rats expression of AT1aR mRNA in the walls of the left and right ventricle of the heart, and in the renal cortex and renal medulla was determined by semiquantitative PCR method. In another group of 10 infarcted and 14 sham-operated rats the diameter of cardiomyocytes in the left and right cardiac ventricle was determined. The size of the infarct in the rats used for mRNA determination and for morphometric measurements was equal to 29.4 +/- 1.8% and to 31.0 +/- 1.2 % of the left ventricular wall, respectively. Expression of AT1aR mRNA was significantly greater in the left (P< 0.01) and right ventricle (P<0.03) of the heart in the infarcted than in the sham operated rats. AT1aR mRNA expression was also significantly greater (P<0.02) in the renal medulla of the infarcted rats than in the renal medulla of the sham operated rats whereas no significant difference was found in the renal cortex. The myocardial infarct was associated with a significant increase of diameter of cardiomyocytes of the left ventricle of the heart (P< 0.0001), however there was no significant correlation between changes in AT1aR mRNA expression and diameter of cardiomyocytes. The results provide evidence that the myocardial infarct results in significant and prolonged upregulation of AT1a receptors mRNA expression in the heart and in the medullary region of the kidney.
authors.affiliation: Department of Experimental and Clinical Physiology, Medical University of Warsaw, Poland.
authors.forename: E
authors.initials: E
authors.lastname: Milik
authors.forename: E
authors.initials: E
authors.lastname: Szczepańska-Sadowska
authors.forename: A
authors.initials: A
authors.lastname: Cudnoch-Jedrzejewska
authors.forename: J
authors.initials: J
authors.lastname: Dobruch
authors.forename: M
authors.initials: M
authors.lastname: Morton
authors.forename: L
authors.initials: L
authors.lastname: Koperski
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D006352:Heart Ventricles / Q000378:metabolism; D006651:Histocytochemistry; D007679:Kidney Medulla / Q000378:metabolism*; D008297:Male; D023421:Models, Animal; D009203:Myocardial Infarction / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000166:cytology; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1