The renin angiotensin aldosterone system in rabbits with congestive heart failure produced by aortic constriction

Abstract

Severe constriction of the suprarenal abdominal aorta of 3 kg rabbits to 3.7 ± 0.2 mm2 and maintenance of a daily sodium intake of 10 mEq by infusion of 0.9% sodium chloride resulted in a progressive increase in central ear arterial pressure to 106 ± 3 (SEM) mm Hg (control = 79 ± 1). This was accompanied by a progressive increase in left ventricular end diastolic pressure to 22 ± 2 mm Hg (control = 3 ± 1), plasma renin activity to 21 ± 5 ng of angiotensin/hour per ml (control = 5 ± 1), plasma aldosterone concentration to 99 ± 23 pg/ml (control = 14 ± 4), and plasma sodium concentration to 142 ± 1 mEq/liter (control = 136 ± 1). Urinary excretion of sodium decreased to 3.9 ± 0.7 mEq/day and marked fluid retention occurred. We also found that these changes were accompanied by a decrease in hematocrit to 24 ± 2% (control = 40 ± 1), the formation of 36 ± 9 ml of fluid in the thoracic cavity, 33 ± 9 ml of ascites, pulmonary congestion and edema, hepatic congestion, and enlargement and hypertrophy of both the left and right ventricles. All rabbits died of ventricular failure at a time that was partly related to the degree of aortic constriction and that ranged from 2 to 12 days. The model we have established is chronic, highly reproducible, easy to produce, and inexpensive, and resembles the clinical syndrome of right and left congestive heart failure in man. Furthermore, the studies provide evidence for an important role of the renin angiotensin aldosterone system in the fluid retention that leads to pulmonary and systemic venous congestion after suprarenal aortic constriction.