Obesity-induced hypertension, like all forms of experimental and human hypertension studied thus far, is associated with renal dysfunction characterized by the resetting of pressure natriuresis. In obese subjects, this resetting is primarily a result of increased renal tubular reabsorption as glomerular filtration rate and renal blood flow are markedly elevated. Obesity activates the sympathetic nervous and renin-angiotensin systems, and causes insulin resistance and hyperinsulinemia, all of which have been postulated to increase tubular reabsorption and raise blood pressure. In humans and dogs, chronic hyperinsulinemia, comparable to that found in obesity, does not cause hypertension even in the presence of insulin resistance. Activation of the sympathetic nervous system appears to be important in obesity, as chronic adrenergic blockade or renal denervation greatly ameliorates the hypertension associated with weight gain. Resetting of pressure natriuresis in obesity may also be attributable to altered intrarenal forces caused by histologic changes in the renal medulla that may compress the loops of Henle and vasa recta, increase tubular sodium reabsorption, and activate the renin-angiotensin system. The quantitative importance of these intrarenal changes and their interrelationship with neurohumoral activation in obesity is an important area for further investigation.