Description:
Elevated dietary NaCl intake enhances both sympathoexcitatory and sympathoinhibitory responses evoked from the rostral ventrolateral medulla. These enhanced responses are prevented by prior lesion of the LT. The purpose of the present study was to test whether increased dietary NaCl intake enhanced a number of sympathetic reflexes dependent on neurotransmission in the rostral ventrolateral medulla and whether this was prevented by LT lesion. Male Sprague‐Dawley rats were fed 0.1% (low) or 4.0% (high) NaCl for 14‐18 days. Electrical stimulation of sciatic afferent nerves (1ms, 1‐20Hz, 500 uA) produced greater increases in renal SNA (5 Hz: 125±9% vs 187±23%, n=6/group) and mean ABP (5Hz: 14±2mmHg vs 28±2mmHg, n=6/group) of rats ingesting high versus low NaCl, respectively. LT lesion prevented the enhanced responses of renal SNA (low: 129±13% vs high: 144±13%, n=3/group) and mean ABP (low: 17±2mmHg vs high: 14±5mmHg, n=5/group). Stimulation of the aortic depressor nerve (1ms, 1‐20 Hz, 500 uA) produced greater decreases in renal SNA (low: ‐53±10% vs high: ‐74±7%, n=6/group) and mean ABP (low: ‐16±3mmHg vs high: ‐32±3mmHg, n=6/group) of rats fed low versus high NaCl diets. Again, LT lesion prevented the enhanced responses of renal SNA (low: ‐58±10% vs high: ‐59±6%, n=3/group) and mean ABP (low: ‐18±5mmHg vs high: ‐15±3mmHg, n=3/group). Similar findings were observed for additional reflexes including activation of vagal afferents and intracerebroventricular infusion of 1M NaCl. These findings suggest dietary salt activates LT neurons to alter the responsiveness of hindbrain neurons and enhance sympathetic reflexes.Grant Funding Source: Supported by NIH R01HL113270 and AHA Established Investigator Award