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1 Pharmacodynamics, University of Florida, Gainesville, FL, USA
* To whom correspondence should be addressed. E-mail: katovich{at}cop.ufl.edu.
Cardiac remodeling is a hallmark hypertension-induced pathophysiology. In the current study, the role of the angiotensin-(1-7) fragment in modulating cardiac remodeling was examined. Sprague-Dawley rats underwent uninephrectomy surgery and were implanted with a deoxycorticosterone acetate pellet (DOCA). DOCA animals had their drinking water replaced with 0.9% saline solution. A subgroup of DOCA-salt animals was implanted with osmotic minipumps, which delivered angiotensin-(1-7) chronically (100 ng/kg/min). Control animals underwent sham surgery and were maintained on normal drinking water. Blood pressure (BP) was measured weekly using a tail-cuff method, and after four weeks of treatment, BP responses to graded doses of angiotensin II were determined by direct carotid artery cannulation. Ventricle size was measured and cross-sections of the heart ventricles were paraffin embedded and stained using Massons Trichrome to measure interstitial and perivascular collagen deposition and myocyte diameter. DOCA-salt treatment caused significant increases in blood pressure, cardiac hypertrophy, and myocardial and perivascular fibrosis. Angiotensin-(1-7) infusion prevented the collagen deposition effects without any effect on blood pressure or cardiac hypertrophy. These results indicate that angiotensin-(1-7) selectively prevents cardiac fibrosis independent of blood pressure or cardiac hypertrophy in the DOCA-salt model of hypertension.
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