1. To test the influence of a sodium (Na+) stimulus within the central nervous system on the release of atrial natriuretic peptide (ANP), we examined the effects of intracerebroventricular infusion of high Na+ artificial cerebrospinal fluid (CSF) on blood pressure, urinary Na+ excretion and plasma ANP levels in conscious Wistar rats.

2. Infusion of high Na+ (0.6 mol/1) CSF into the lateral ventricle at a rate of 1 μl/min for 60 min significantly increased mean blood pressure and urinary Na+ excretion, while normal Na+ (0.15 mol/1) CSF had no effects. Plasma ANP levels were higher in the high Na+ CSF group than in the normal Na+ group (154 ±39 vs 52 ±19 pmol/l, P < 0.05).

3. Interruption of the sympathetic nervous system and the vascular action of vasopressin with intravenous hexamethonium and d(CH2)5Tyr(Me)arginine vasopressin attenuated the pressor and natriuretic responses to intracerebroventricular high Na+ CSF. Plasma ANP levels in these rats did not differ significantly from those in rats which were similarly treated but were given normal Na+ CSF.

4. These results indicate that elevation of the CSF Na+ concentration without peripheral volume loading can stimulate ANP release into the circulation. ANP release due to central Na+ stimulus appears to be mediated by the sympathetic nervous system, vasopressin, and/or haemodynamic change caused by these factors.

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