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

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Abstract
The natriuretic response to intravenous infusion of 2 M-NaCl was investigated in six conscious sheep. This hypertonic NaCl load resulted in relatively small, physiological (2-3 mmol l-1) increases in plasma Na+ concentration and was followed by a natriuresis with a maximum mean urinary sodium excretion 5 times higher than pre-infusion values. Intravenous infusion of isotonic NaCl, delivering the same Na+ load as hypertonic NaCl infusion, did not induce natriuresis. This suggested, therefore, that with the hypertonic sodium load administered in the present study, the rise in plasma Na+ and/or tonicity rather than increase in blood volume is important in evoking the natriuretic response. Intracerebroventricular infusion of low-Na+ artificial cerebrospinal fluid (CSF) reduced CSF Na+ concentration, decreased plasma vasopressin (AVP) levels and caused a copious water diuresis. This was associated with excessive loss of water and large increases in plasma Na+ concentration and osmolality. The natriuresis induced by intravenous hypertonic NaCl load could be blocked by lowering CSF Na+ concentration in situations where water diuresis was either prevented or reduced by intravenous infusion of AVP or by delayed intracerebroventricular infusion of low-Na+ CSF, respectively. The results of the present study provide further evidence that renal sodium excretion can be controlled by the central nervous system.