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On the importance of CSF Na in the regulation of renal sodium excretion and renin release

1982; Wiley; Volume: 115; Issue: 1 Linguagem: Inglês

10.1111/j.1748-1716.1982.tb07056.x

1365-201X

L. G. Leksell, Derek A. Denton, D. T. W. Fei, M. J. McKinley, A. F. Muller, R. S. Weisinger, Heather M. Young,

Ion Transport and Channel Regulation

Infusions (20 μl/min) of isotonic (0.27 M) mannitol dissolved in Na‐free artificial cerebrospinal fluid (CSF) were made for 2 h into the lateral cerebral ventricle (IVT) of conscious 68 h dehydrated sheep. The IVT infusion induced a conspicuous drop in renal sodium excretion and marked rise in plasma renin concentration (PRC). The antinatriuretic response to the IVT. infusion was not altered by the intravenous: administration of ADH or the converting enzyme blocker (SQ 14225, Captopril). Surgical bilateral renal denervation did not change the antinatriuretic response while the increase in PRC was extinguished. Samples of CSF were collected prior to, and 15 min after the end of the infusion. These showed a reduction in CSF.[Na], while CSF osmolality remained unchanged. The study supports the view that sodium sensitive receptors close to the cerebral ventricular system participate in the regulation of renal sodium excretion and renin release, it also suggests that renal sodium excretion is affected by an unknown hormonal factor of cerebral origin, while the release of renin seen in response to a reduction in CSF [Na] is mediated by the renal nerves.