Dietary salt intake exaggerates sympathetic reflexes and increases blood pressure variability in normotensive rats

摘要

Previous studies have reported that chronic increases in dietary salt intake enhance sympathetic nerve activity (SNA) and arterial blood pressure (ABP) responses evoked from brainstem nuclei of normotensive, salt-resistant rats. The purpose of the present study was to determine whether this sensitization results in exaggerated SNA and ABP responses during activation of various cardiovascular reflexes and also increases ABP variability (BPV). Male Sprague-Dawley rats were fed 0.1% NaCl chow (low), 0.5% NaCl chow (medium), 4.0% NaCl chow (high) for 14–17 days. Then, animals were prepared for recordings of lumbar, renal, and splanchnic SNA and ABP. The level of dietary salt intake directly correlated with the magnitude of SNA and ABP responses to electrical stimulation of sciatic afferents or intracerebroventricular infusion of 0.6M or 1.0M NaCl. Similarly, there was a direct correlation between the level of dietary salt intake and the sympathoinhibitory responses produced by acute volume expansion, stimulation of the aortic depressor nerve or cervical vagal afferents. In contrast, dietary salt intake did not affect the sympathetic and ABP responses to chemoreflex activation produced by hypoxia or hypercapnia. Chronic lesion of the anteroventral 3^rd ventricle region eliminated the ability of dietary salt intake to modulate these cardiovascular reflexes. Finally, rats chronically instrumented with telemetry units indicate that increased dietary salt intake elevated BPV but not mean ABP. These findings indicate that dietary salt intake works through the forebrain hypothalamus to modulate various centrally-mediated cardiovascular reflexes and increase BPV.