1. The present studies are designed to determine whether a ouabain-sensitive inhibitor of Na+, K+−stimulated ATPase is released into the circulation when the Na+ levels are elevated in the cerebral ventricles in pentobarbital anaesthetized dogs. Na+−pump activity was estimated in the plantar and dorsal branches of the lateral saphenous veins by using the 86Rb-uptake method.

2. Infusion of the cerebral ventricles with the artificial cerebrospinal fluid (CSF) containing normal Na+ (0.15 mol/l) for over 120 min resulted in significant increases in only ouabain-sensitive 86Rb-uptake. In contrast, when the ventricles were perfused with the CSF containing high Na+ (0.3 mol/l) for similar periods, there were significant reductions in the ouabain-sensitive as well as in ouabain-insensitive 86Rb-uptake by the blood vessels.

3. Similar blood vessels from a separate group of dogs were incubated for 120 min in the plasma samples collected from the above groups in which normal or hypertonic Na+ solutions were infused. The data showed that ouabain-sensitive 86Rb-uptake (but not the insensitive component) was significantly inhibited only in those vessels which were incubated in the plasma samples that were obtained at 120 min after perfusion of the cerebral ventricles with CSF containing high Na+ (0.3 mol/l).

4. These studies have provided direct evidence which would suggest that the elevation of Na+ levels in the cerebral ventricles would precipitate the release of an inhibitor of the ouabain-sensitive Na+−pump into the circulation, perhaps due to an activation of Na+−sensitive and/or osmo-sensitive sites in the circumventricular organs. It is hypothesized that this humoral substance may be the same ‘natriuretic hormone’ which is released after acute expansion of circulating blood volume.

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