Neurogenic regulation of rate of achieving sodium balance after increasing sodium intake

Evidence that the renal sympathetic nerves have direct effects on renal tubular function suggests that neurogenic mechanisms may play an important role in the daily regulation of sodium balance. We evaluated the influence of the renal nerves on the rate of elevating urinary sodium excretion (U_NaV) after a step increase in fixed sodium intake. Conscious rats with innervated (INN) or denervated (DNX) kidneys were placed on low-sodium intake (LNa = 0.3 meq/day) or a normal sodium intake (NNa = 1.0 meq/day) by intravenous infusion. Hourly changes in U_NaV were determined 24 h before and 72 h after increasing sodium intake to either NNa or high-sodium intake (HNa = 5.0 meq/day). Switching from LNa to NNa, INN rats increased U_NaV within 24 h; however, DNX rats did not begin to increase U_NaV until hour 60. Cumulative sodium balance over 72 h was more positive in DNX rats (INN = 1.29 ± 0.29 meq; DNX = 2.06 ± 0.21 meq, P < 0.05). During the LNa-to-HNa switch, both INN and DNX rats increased U_NaV equally for 12 h; however, at this time INN rats continued to increase U_NaV, whereas DNX rats did not. DNX rats had a net accumulation of 2.54 meq more sodium than INN rats over 72 h. Significant inhibition of plasma renin activity within the first 24 h occurred only in rats receiving the LNa-to-HNa switch in sodium intake, and this response was not different between rats with innervated and denervated kidneys. These data suggest that the renal nerves provide a rapid sodium excretory response to step increases in sodium intake. Renal sympathetic outflow may serve as a rapid controller of the onset of maintaining normal sodium balance.