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

Abstract

Infusions (20 microliters/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 te 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.

Hypothalamic integration of body fluid regulation.

“…Reduction of CSF [Na] increases plasma renin levels in dogs (71) and sheep (72), whereas an increase in the tonicity of carotid arterial blood reduces it in conscious sheep, an effect abolished by ablation of the lamina terminalis (73). Consequently, we have proposed that there is an inhibitory cerebral osmoregulatory influence on renin secretion by the kidney (73).…”

Cerebral regulation of renal sodium excretion in sheep infused intravenously with hypertonic NaCl.

“…The kidney responded to this infusion within an Nour. The antinatriuretic response was not mediated by renal nerves nor were changes observed in glomerular filtration rate or renal blood flow when CSFNa was lowered (Leksell et al 1982;McKinley et al 1983b A. CHODOBSKI AND M. J. McKINLEY observed despite the increases in PRC and inhibition of angiotensin-converting enzyme had no effect on the antinatriuresis (Leksell et al 1981(Leksell et al , 1982. In the present study, statistically significant increases in PRC during I.c.v.…”

“…This natriuresis has also been observed to be inhibited by i.c.v. infusion of low-Na+ CSF in sheep deprived of water for 1-3 days (Leksell et al 1981(Leksell et al , 1982McKinley et al 1983 b). The kidney responded to this infusion within an Nour.…”

Cerebral Mechanisms Influencing Renal Sodium Excretion in Dehydrated Sheep

“…The present results tend to rule out generalized haemodynamic changes as the cause because arterial blood pressure, cardiac rate, GFR and ERPF were unaltered. it is possible that neural and/or hormonal pathways may be involved in this antinatriuresis although it is unlikely that the effect is mediated by changes in renal nerve activity because such an antinatriuresis was still observed in sheep with denervated kidneys (Leksell et al, 1982). With regard to humoral factors subserving the reduced Na excretion, although a significant reduction in the Na/K ratio of the urine was observed in the latter stages of the mannitol infusion (Table I), the rapidity of the antinatriuresis indicates that a nonmineralocorticoid mechanism was probably operative in the initial part of the response.…”