We have previously demonstrated blunted reflex responses of lumbar sym
pathetic nerve activity during volume expansion in NaCl-sensitive spon
taneously hypertensive rats maintained on basal (1% NaCl) diets compar
ed with NaCl-resistant spontaneously hypertensive rats, Wistar-Kyoto r
ats, and Sprague-Dawley rats. The current study tested the hypothesis
that chronic ingestion of a high (8%) NaCl diet further blunts cardiop
ulmonary reflex function in the NaCl-sensitive spontaneously hypertens
ive 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 an
d 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% NaC
l diet had blunted responses of nerve activity to acute volume expansi
on compared with control strains. NaCl-sensitive spontaneously hyperte
nsive rats maintained on an 8% NaCl diet had increases in nerve activi
ty responses to volume expansion. In a second experiment, the volume e
xpansion protocol was repeated in anesthetized NaCl-sensitive spontane
ously hypertensive rats that had been subjected to sinoaortic denervat
ion after 3 weeks of a 1% or 8% NaCl diet. After sinoaortic denervatio
n, an increase in nerve activity was again observed during volume expa
nsion 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 hypert
ensive rats is a complex interaction of excitatory and inhibitory symp
athetic reflex systems that is altered by high dietary NaCl exposure.