Hypertension, Vol 24, 571-575, Copyright © 1994 by American Heart Association
W Wang
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 micrograms/kg in 2 mL) 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 micrograms/kg i.v.).(ABSTRACT
TRUNCATED AT 250 WORDS)
ARTICLES
Chronic administration of aldosterone depresses baroreceptor reflex function in the dog
Department of Physiology and Biophysics, University of Nebraska, College of Medicine, Omaha 68198-4575.
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