Elevation of CSF sodium concentration without peripheral volume loading stimulates ANP release into the circulation, likely mediated by the sympathetic nervous system and vasopressin.
Central sodium sensing may drive ANP release independently of volume; leaves open relevance to human HF or hypertension.
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/l) CSF into the lateral ventricle at a rate of 1 microliter/min for 60 min significantly increased mean blood pressure and urinary Na+ excretion, while normal Na+ (0.15 mol/l) 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 less than 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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Kawano et al. (1988) studied this question.
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