Hypertension occurs more frequently in U.S. blacks than whites and is more severe. Blacks represent a disproportionate percentage of patients receiving dialysis treatment. This disproportion raises the question of whether the renal circulation of blacks is more sensitive to the damaging effects of elevated intraarterial pressure or whether it is structurally different in ways that would render it more prone to damage. The first part of the question has not been conclusively answered although some data support the hypothesis. For the second part, it is clear that malignant nephrosclerosis of blacks is different from that of whites in an absence of fibrinoid necrosis of arterioles and glomeruli and the presence of musculomucoid intimal hyperplasia of small arteries. Whether this is a genetically determined reaction to damage has not been determined. It is a widely held belief that the kidney is the cause of much essential hypertension. In fact 6 cases of essential hypertension in blacks have been "cured" by renal transplantation, strongly supporting the belief. Also blacks differ from whites in 2 ways that could be relevant for their increased prevalence of hypertension: they excrete sodium loads more slowly and have a markedly lower urinary kallikrein. The former could be responsible for the predominance of salt-dependent hypertension in blacks and the latter could reflect a racial deficiency in a naturally occurring vasodilator system.