on March 18, 2002
Circulation. 2002
Published online before print March 18, 2002, doi: 10.1161/01.CIR.0000013847.07035.B9
Published online before print March 18, 2002, doi: 10.1161/01.CIR.0000013847.07035.B9
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Submitted on December 13, 2001
From the Department of Clinical Pharmacology, University of Groningen (A.E.L., A.J.M.R., R.H.H., W.H.v.G.); Departments of Cardiology (R.A.T., W.H.v.G.) and Pathology (A.J.H.S.), University Hospital Groningen; and Department of Internal Medicine, Erasmus University Medical Center, Rotterdam (F.B.), the Netherlands. * To whom correspondence should be addressed. E-mail: a.e.loot{at}med.rug.nl.
Background—The renin-angiotensin system (RAS) is a key player in the progression of heart failure. Angiotensin-(1--7) is thought to modulate the activity of the RAS. Furthermore, this peptide may play a part in the beneficial effects of angiotensin-converting enzyme inhibitors in cardiovascular disease. We assessed the effects of angiotensin-(1--7) on the progression of heart failure. Methods and Results—Male Sprague-Dawley rats underwent either coronary ligation or sham surgery. Two weeks after induction of myocardial infarction, intravenous infusion of angiotensin-(1--7) (24 µg/kg per hour) or saline was started by minipump. After 8 weeks of treatment, hemodynamic parameters were measured, endothelial function was assessed in isolated aortic rings, and plasma angiotensin-(1--7) levels were determined. Myocardial infarction resulted in a significant deterioration of left ventricular systolic and diastolic pressure, dP/dt, and coronary flow. Raising plasma levels 40-fold, angiotensin-(1--7) infusion attenuated this impairment to a nonsignificant level, markedly illustrated by a 40% reduction in left ventricular end-diastolic pressure. Furthermore, angiotensin-(1--7) completely preserved aortic endothelial function, whereas endothelium-dependent relaxation in aortas of saline-treated infarcted rats was significantly decreased. Conclusions—Angiotensin-(1--7) preserved cardiac function, coronary perfusion, and aortic endothelial function in a rat model for heart failure.
Revised on February 5, 2002
Accepted on February 5, 2002
Angiotensin-(1--7) Attenuates the
Development of Heart Failure After Myocardial Infarction in
Rats
Annemarieke E. Loot MSc*,
Key words: angiotensin • heart failure • hemodynamics • myocardial infarction
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