Hypertension, Vol 14, 518-523, Copyright © 1989 by American Heart Association
RM Thornton, JM Wyss and S Oparil
Abnormal baroreceptor reflex function that antedates or is a consequence of
NaCl loading could contribute to the NaCl-induced exacerbation of
hypertension in NaCl-sensitive spontaneously hypertensive rats (SHR-S). The
current study tested the hypothesis that an impairment in cardiopulmonary
baroreceptor reflex function exists in SHR-S before NaCl loading. The
reflex response to volume expansion was compared in SHR-S, NaCl-resistant
SHR (SHR-R), and normotensive Wistar- Kyoto (WKY) and Sprague-Dawley rats
maintained on a normal NaCl diet. Conscious, free-moving SHR-S, SHR-R, WKY,
and Sprague-Dawley rats were volume expanded with whole blood to 15% of
blood volume within 6 minutes, and mean arterial pressure, heart rate, and
lumbar sympathetic nerve activity were recorded. Heart rate and lumbar
sympathetic nerve activity decreased significantly in SHR-R, WKY, and
Sprague-Dawley rats after volume expansion. In contrast, in SHR-S neither
heart rate after volume expansion nor lumbar sympathetic nerve activity was
significantly different from levels before volume expansion. The blunted
reflex response of heart rate and lumbar sympathetic nerve activity to
volume expansion suggests impaired cardiopulmonary volume receptor function
in SHR-S. This likely contributes to NaCl-induced hypertension in SHR-S on
a high NaCl diet.
ARTICLES
Impaired reflex response to volume expansion in NaCl-sensitive spontaneously hypertensive rats
Department of Medicine, University of Alabama, Birmingham.
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