title: Angiotensin receptor 1 blockade does not prevent physiological cardiac hypertrophy in the adult rat.
abstract: The renin-angiotensin system has been implicated in the hypertrophic adaptation of the heart to exogenous pathological loads, such as hypertension and aortic stenosis; however, the role of this hormonal system in the cardiac adaptations to physiological loads, such as chronic exercise conditioning, has not been established. We therefore studied the effect of angiotensin receptor 1 (AT1) blockade on the chronic cardiac responses of rats subjected to an 8-wk swimming program. Compared with matched sedentary controls, untreated swimmers increased their left ventricular weights by 13%, and swimmers treated with the AT1 antagonist L-158809 increased their left ventricular weights by 11% (both P < 0.05 vs. sedentary controls). The incorporation of labeled amino acids into the heart at the time of death was unchanged in all groups, and therefore the increase in heart weight in both swim-conditioned groups appeared to reflect a decrease in the rate of protein degradation in the heart. Hearts from both swim-conditioned groups manifested an increase in the V1-predominant myosin isoform pattern but not an increase in atrial natriuretic factor mRNA expression or protein kinase C translocation. The fact that these patterns of adaptation are preserved in exercised conditioned animals treated with an AT1 antagonist suggests that the chronic hypertrophic response of the heart to physiological loads is not influenced by the renin-angiotensin system.
authors.affiliation: Division of Cardiology, Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, New York 10467, USA.
authors.forename: D L
authors.initials: DL
authors.lastname: Geenen
authors.forename: A
authors.initials: A
authors.lastname: Malhotra
authors.forename: P M
authors.initials: PM
authors.lastname: Buttrick
mesh_terms: D000803:Angiotensin I / Q000378:metabolism*; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D015152:Blotting, Northern; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D006332:Cardiomegaly / Q000503:physiopathology / Q000517:prevention & control*; D003285:Contractile Proteins / Q000096:biosynthesis; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D007093:Imidazoles / Q000494:pharmacology*; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D009929:Organ Size / Q000187:drug effects / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology; D011493:Protein Kinase C / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013777:Tetrazoles / Q000494:pharmacology*
chemical_list: D057911:Angiotensin Receptor Antagonists; D000959:Antihypertensive Agents; D003285:Contractile Proteins; D007093:Imidazoles; D012333:RNA, Messenger; D013777:Tetrazoles; C070967:L 158809; D000803:Angiotensin I; D011493:Protein Kinase C