Hypertension, Vol 19, 270-277, Copyright © 1992 by American Heart Association
W Wang, JM McClain and IH Zucker
We have previously demonstrated that baroreceptor discharge sensitivity is
depressed in dogs with experimental heart failure and that this depressed
sensitivity can be reversed by the Na+,K(+)-ATPase inhibitor ouabain. This
suggests that enhanced Na+,K(+)-ATPase activity in baroreceptors is
responsible for the blunted baroreceptor discharge sensitivity seen in
heart failure state. Because aldosterone, a known stimulator of
Na+,K(+)-ATPase, is elevated in heart failure the present study was
undertaken to determine the effects on baroreceptor discharge of perfusion
of the carotid sinus with aldosterone in normotensive dogs. Single unit
baroreceptor activity was recorded as well as carotid sinus pressure and
the diameter of the carotid sinus. Perfusion of the carotid sinus with
aldosterone (in Krebs-Henseleit solution) significantly elevated threshold
pressure (108.5 +/- 3.1 mm Hg versus 92.7 +/- 4.6 mm Hg, p less than 0.05)
and reduced peak discharge rate (40.3 +/- 3.9 spikes/sec, p less than
0.05). These effects appeared 15 minutes after aldosterone perfusion and
remained constant for the next 60 minutes. There was no change in the
carotid sinus pressure-diameter curve during perfusion with aldosterone.
Perfusion of the carotid sinus with ouabain (0.1 microgram/ml) during
aldosterone perfusion did not reverse the blunted baroreceptor discharge.
The blunted baroreceptor activity induced by perfusion of the carotid sinus
with aldosterone was prevented by removal of the endothelial cells in the
carotid sinus area with a balloon-tipped catheter or by perfusion with
saponin. Finally, perfusion of the carotid sinus with spironolactone (10
ng/ml), a mineralocorticoid receptor antagonist, prevented the inhibitory
effect of aldosterone. These data suggest that aldosterone reduces maximum
baroreceptor discharge.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Aldosterone reduces baroreceptor discharge in the dog
Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha 68198-4575.
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