Sympathoinhibitory effects of central nifedipine in spontaneously hypertensive rats on high versus regular sodium intake

The putative central sympathoinhibitory actions of the dihydropyridine calc ium antagonist nifedipine and the effect of dietary sodium on these actions were investigated in spontaneously hypertensive rats (SHR). Regular or hig h dietary salt was administered from 4 to 8 weeks of age. At 8 weeks, blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity were recorded in conscious rats at rest as well as in response to intravenous (5 0 mu g/kg) and intracerebroventricular (5 and 50 mu g/kg) injections of nif edipine and intracerebroventricular injections of vehicle. Resting mean art erial pressure was higher in SHR on high versus regular salt (159+/-3 versu s 135+/-4 mm Hg; P<0.05). Nifedipine administered intracerebroventricularly decreased BP as well as renal sympathetic nerve activity and HR in a dose- related manner. The responses reached their peak at 3 to 5 minutes and last ed approximate to 30 minutes. Peak decreases in BP, renal sympathetic nerve activity, and HR in response to both doses of nifedipine were significantl y larger in SHR on high versus regular salt. Nifedipine administered intrav enously also decreased BP but, in contrast, caused (reflex) increases in re nal sympathetic nerve activity and HR. On both diets, intracerebroventricul ar vehicle did not affect mean arterial pressure, renal sympathetic nerve a ctivity, or HR. These data indicate that in contrast to its peripheral vaso dilator effect, centrally administered nifedipine may decrease sympathetic outflow and therefore BP and HR. The enhanced sympathoinhibitory and depres sor responses to nifedipine in SHR on high versus regular salt suggest that the sympathetic hyperactivity induced by high salt intake is dependent on neuronal calcium influx via L-type channels.