Hypertension, Vol 22, 285-291, Copyright © 1993 by American Heart Association
Y Nakamura, DA Calhoun, YF Chen, JM Wyss and S Oparil
We have previously demonstrated blunted reflex responses of lumbar
sympathetic nerve activity during volume expansion in NaCl-sensitive
spontaneously hypertensive rats maintained on basal (1% NaCl) diets
compared with NaCl-resistant spontaneously hypertensive rats, Wistar- Kyoto
rats, and Sprague-Dawley rats. The current study tested the hypothesis that
chronic ingestion of a high (8%) NaCl diet further blunts cardiopulmonary
reflex function in the NaCl-sensitive spontaneously hypertensive rat. After
3 weeks of a 1% or 8% NaCl diet, male rats of all four strains were
instrumented with femoral arterial and venous cannulas and lumbar nerve
recording electrodes at 10 weeks of age. Two days later, conscious rats
were infused with whole blood to expand blood volume. NaCl-sensitive
spontaneously hypertensive rats maintained on a 1% NaCl diet had blunted
responses of nerve activity to acute volume expansion compared with control
strains. NaCl-sensitive spontaneously hypertensive rats maintained on an 8%
NaCl diet had increases in nerve activity responses to volume expansion. In
a second experiment, the volume expansion protocol was repeated in
anesthetized NaCl-sensitive spontaneously hypertensive rats that had been
subjected to sinoaortic denervation after 3 weeks of a 1% or 8% NaCl diet.
After sinoaortic denervation, an increase in nerve activity was again
observed during volume expansion in animals fed the 8% NaCl diet. In
animals fed the 1% NaCl diet, changes in nerve activity were variable. The
excitatory response was significantly reduced after bilateral vagotomy.
These studies suggest that blood pressure regulation in NaCl- sensitive
spontaneously hypertensive rats is a complex interaction of excitatory and
inhibitory sympathetic reflex systems that is altered by high dietary NaCl
exposure.
ARTICLES
Excitatory sympathetic reflex in NaCl-sensitive spontaneously hypertensive rats
Department of Medicine, University of Alabama, Birmingham 35294.
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