CHRONIC ADMINISTRATION OF ALDOSTERONE DEPRESSES BARORECEPTOR REFLEX FUNCTION IN THE DOG

In a previous study it was shown that acute perfusion of aldosterone into the isolated carotid sinus decreased baroreceptor activity. The aim of the present study was to determine whether chronic, systemic administration of aldosterone also depresses baroreflex function. In six conscious dogs, the baroreflex was determined before and 10 days after an osmotic minipump containing aldosterone (100 mu g/kg in 2 mt) was implanted. The slope of the relation between systolic arterial pressure and heart rate was significantly blunted after aldosterone administration (9.1+/-0.7 versus 13.3+/-1.2 for nitroglycerin, P<.01; 23.4+/-5.0 versus 40.1+/-5.0 for phenylephrine, P<.01). Baroreflex slopes did not change in a sham group (minipump with saline) and an aldosterone plus spironolactone (600 mg/d) group. Plasma aldosterone levels were significantly elevated after the aldosterone minipump was implanted (443+/-72 versus 37+/-11 pg/mL, P<.001). Mean arterial pressure was not significantly increased after aldosterone (106.5+/-3.8 versus 100.4+/-2.6 mm Hg, P=.2). On the 10th day after aldosterone or saline infusion, an acute experiment was carried out. Single baroreceptor fibers were recorded from the carotid sinus nerve. Compared with the sham group, the threshold was significantly elevated in the aldosterone group (111.3+/-2.1 versus 85.8+/-2.8 mm Hg), and the peak discharge rate was markedly decreased (32.5+/-1.5 versus 54.7+/-2.5 spikes per second, P<.01). The depressed baroreceptor function could be partially restored after a bolus injection of the Na+,K+-ATPase inhibitor ouabain (5 mu g/kg IV). These data indicate that chronic administration of aldosterone decreases baroreflex function without inducing hypertension. An Na+,K+-ATPase mechanism is involved in this aldosterone-induced depression of baroreceptor function. This mechanism may be involved in the blunting of the baroreflex in heart failure and other hyperaldosteronemic states.