Abstract

Compelling evidence indicates that excess dietary salt enhances sympathetic nerve activity (SNA) and arterial blood pressure (ABP) responses evoked from the rostral ventrolateral medulla (RVLM). The present study investigated whether excess dietary salt selectively enhances the excitability of RVLM neurons vs all sympathetic‐regulatory networks. Male Sprague‐Dawley rats were given access to water or 0.9% NaCl for 15‐18 days. Rats drinking 0.9% NaCl (n=5) vs water (n=6) had significantly greater increases in renal SNA (62±7 vs 40±6%, P<0.05) and mean ABP (27±4 vs 12±3mmHg, P<0.01) during electrical stimulation of sciatic afferents (500 μA, 2Hz). In marked contrast, injection of L‐glutamate (5nmol/100nL) into the medullo‐cervical pressor area produced similar increases in renal SNA (110±20% vs 133±21%) and mean ABP (25±4 vs 25±4mmHg) of rats drinking 0.9% NaCl vs water. Inhibition of the RVLM with muscimol (500 pmol/side, n=3) eliminated the increased renal SNA (45±8 vs 0±0%) and mean ABP (13±2 vs 1±1mmHg; P<0.01) to sciatic nerve stimulation, but did not affect renal SNA (95±9 vs 88±10%) or mean ABP (18±4 vs 19±5mmHg) to glutamatergic stimulation of the medullo‐cervical pressor area. The potentiated increases in renal SNA and ABP to only RVLM‐dependent responses suggest that excess dietary salt selectively enhances the excitability of RVLM sympathetic neurons. Supported by NIH HL090826, AHA 0630202N

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