Here we have reviewed mainly the cerebral regulation of water intake and its relationship with the regulation of the water-retaining antidiuretic hormone (ADH). Much new information of obvious interest has been gained by experiments in conscious animals, by studies in healthy humans, and by clinical investigations. Of particularly great value has been the development of a sensitive radioimmunoassay for determination of plasma ADH (59). The sketchy picture that emerges in light of this new information is as follows. The osmotic regulation of water intake and ADH secretion is exerted by juxtacerebroventricular sensors apparently mainly located on the anterior border of the third ventricle. These sensors may be accessible both to CSF-borne and blood-borne stimuli and inhibitors, and their activity seems to be correlated to the Na concentration of the ECF rather than to its tonicity. A less sensitive volume regulation of water intake and ADH secretion is effectuated by cardiovascular distention and pressure receptors monitoring the effective circulating blood volume, and in severe volume depletion states also by the renin-angiotensin system (RAS). Afferent impulses from the cardiovascular receptors exert a tonic inhibition of the ADH release by acting upon its final neuronal link (the cells of the supraoptic and paraventricular nuclei). Afferent inflow from these receptors also inhibits thirst to some extent, perhaps by preventing at some synaptic level information from cerebral "thirst" sensors from reaching other parts of the brain where the information is converted into a conscious urge to drink. Therefore, increased cardiovascular receptor activity becomes manifested as elevated osmotic thresholds for ADH liberation and thirst. Severe volume depletion may induce RAS hyperactivity to such an extent that generated angiotensin II stimulates the ADH release and water intake. Demonstrated cerebral Na/angiotensin interaction suggests that this may occur via an angiotensin-induced lowering of the stimulus threshold for the sensors involved in the osmotic control of water balance. Cerebral damage affecting the sensors responsible for the osmotic regulation of water intake and ADH release may result in hypo- or adipsia associated with latent diabetes insipidus, and is apparently the ultimate cause of "essential" hypernatremia. This fragmentary outline of the cerebral control of water intake is based to a considerable extent upon circumstantial evidence, and is for that reason speculative on many points.