This paper summarizes the role of the renal pressure natriuresis and diuresis mechanisms in maintaining sodium and water balance in hypertension. In all forms of chronic hypertension studied to date, the renal pressure natriuresis and diuresis mechanisms are abnormal, since increased arterial pressure is required to maintain normal excretion of sodium and water, and therefore fluid balance. When renal perfusion pressure is prevented from increasing in various forms of experimental hypertension, caused by infusion of mineralocorticoids, angiotensin II, vasopressin, or norepinephrine and adrenocorticotrophic hormone (ACTH), sodium and water retention continues until ascites, pulmonary oedema and circulatory collapse occur within a few days. Thus, chronic hypertension appears to be an essential homeostatic response that permits sodium and water balance to be maintained despite various abnormalities which tend to decrease renal excretory capability. The intrarenal mechanisms by which increased renal perfusion pressure maintains sodium and water balance in hypertension have not been fully elucidated, but appear to involve small changes in glomerular filtration rate (GFR) and reductions in fractional sodium reabsorption, due either to the direct hydraulic effects of pressure or to various indirect effects, such as changes in angiotensin II formation.