Abstract
The evidence that the natriuresis in response to such hemodynamic alterations as infusion of saline or blood and carotid occlusion is related to the appearance of a natriuretic activity in the plasma was reviewed. This activity, which can be assayed by tubular rejection of sodium in the hydrated ethanol-anesthetized rat or chloralosed cat, or by the zero potential current method in frog skin, was most prominent in blood from the internal jugular vein and then the femoral artery; no such activity was found in blood from the renal or femoral veins. It was therefore postulated that this activity is of cerebral origin. Extracts of posterior bovine hypothalamus when treated with proteolytic enzymes first showed an antinatriferic action, which disappeared on longer incubation. This activity is presumably contained in a polypeptide which is present in a larger "hormonogen" molecular form in the posterior hypothalamus; destruction of the posterior hypothalamus results in renal loss of sodium. Some questions remain: are the natriuretic and antinatriferic activities properties of the same substance; and do the activities that have been obtained from the posterior hypothalamus and plasma represent the same substance?