AJP - Heart and Circulatory Physiology, Vol 247, Issue 1 119-H123, Copyright © 1984 by American Physiological Society
Impairment of cardiopulmonary baroreflexes in Dahl salt-sensitive rats fed low salt
A. Ferrari, F. J. Gordon and A. L. Mark
Abnormalities in neural circulatory control contribute to salt-induced
hypertension in Dahl sensitive (DS) rats. This study tested the hypothesis
that there is impairment in cardiopulmonary baroreflex function in
prehypertensive DS rats. The study was performed in DS and Dahl resistant
(DR) rats fed low-salt diet. Arterial baroreceptors were denervated.
Sympathetic activity was recorded from the splanchnic nerve during
stimulation of cardiopulmonary baroreceptors with volume expansion (iv
dextran). Resting mean arterial pressure averaged 93 +/- 6 (SE) in DS vs.
98 +/- 5 mmHg in DR rats. Resting left ventricular end-diastolic pressure
(LVEDP) was 13.5 +/- 1.0 in/DS vs. 11.4 +/- 0.9 mmHg in DR rats. Volume
expansion with the same amount of dextran caused greater increases in LVEDP
in DS (+13 +/- 1 mmHg) than DR (+10 +/- 1 mmHg) but less inhibition of
sympathetic activity (-40 +/- 4 vs. -50 +/- 2%) in DS compared with DR
rats, respectively. Cardiopulmonary baroreflex gain calculated as percent
inhibition of sympathetic activity divided by increases in LVEDP was -3.2
+/- 0.2 in DS vs. -4.9 +/- 0.6%/mmHg in DR rats. Reflex responses to
dextran were abolished by vagotomy. Volume expansion also induced increases
in mean arterial pressure. These were/greater in DS than DR rats (+43 +/- 4
vs. +28 +/- 5 mmHg, respectively) before vagotomy but were similar in the
two groups after vagotomy. The distensibility (delta volume/delta pressure)
of the left atrium was similar in DS and DR rats. We conclude that
prehypertensive DS rats have impairment of the cardiopulmonary
baroreflex.(ABSTRACT TRUNCATED AT 250 WORDS)
