CNS‐induced natriuresis is not mediated by the atrial natriuretic factor

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Abstract
Studies were performed on anaesthetized Wistar‐Kyoto rats to investigate whether the natriuretic response to stimulation of the cerebroventricular system with a hypertonic sodium solution is in part caused by increased plasma concentrations of atrial natriuretic factor (ANF).Through a cannula inserted into a lateral cerebral ventricle a solution with a normal (CSF, 152 mmoll‐1) or high (NaCSF, 1000 mmoll‐1) sodium ion content was infused. In the stimulated animals which received NaCSF, the sodium excretion increased more than 13‐fold, from 0.07 ± 0.02 (mean ± SEM) to 0.97 ± 0.22 μmol min‐1 g‐1 kidney wt (P < 0.01).Potassium excretion rose more than eight‐fold, from 0.37 ± 0.05 103.01 ± 0.13 μmol min‐1 g‐1 kidney wt (P < 0.001), and the urine flow rate more than seven‐fold, from 1.35±0.11 to 9.74±1.23μ min‐1 g‐1 kidney wt (P < 0.001).The mean arterial blood pressure increased from 100 ± 3 to 129±17 mmHg (P < 0.001).In the control animals which received CSF throughout the experiment there was no significant change in the above variables. The concentrations of ANF in plasma taken at the end of the experiments were determined by a radioimmunoassay. The mean plasma concentration of ANF in animals receiving CSF throughout the experiment was 175 ± 36 pg ml‐1.This was not significantly different from the corresponding value in animals which were given NaCSF (118 ± 34 pg ml‐1).In conclusion, stimulation of the cerebroventricular system with a hypertonic sodium solution induced marked increases in electrolyte excretion. The results of this study indicate that this effect is mediated by some other factor than ANF.