Evidence suggests that the incidence of renal failure due to hypertension is higher in Afro-Americans than in white patients. It has been proposed that, for any given level of blood pressure, the renal circulation of Afro-Americans, may be more susceptible to the injury of hypertension. The hypothesis to be tested in these studies is that the greater prevalence of renal failure in black hypertensives might be due to a derangement of the mechanisms regulating the microvascular renal circulation, particularly in response to a high sodium diet. This derangement would lead to an increase in intraglomerular pressure and to progressive glomerular sclerosis and renal failure. To test this hypothesis a group of male or female blacks with hypertension and a group of age matched white patients, will be studied in a metabolic ward, while ingesting a diet with low or high content of salt. The effect of different sodium diet on plasma and urinary catecholamines, urinary prostaglandins, and on renal hemodynamics will be evaluated. In addition, antagonists of norepinephrine, angiotensin II, vasodilator prostaglandins, and thromboxane, will be used to determine the influence of these hormones on the renal microcirculation, in black salt-sensitive as compared with salt-resistant hypertensive patients. Finally, we plan to measure urinary albumin excretion in salt-sensitive and in salt-resistant patients, and to correlate the amount of proteinuria with salt-sensitivity and the renal hemodynamic changes. These studies may provide new insights into the link between hypertension and renal failure in Afro-Americans, and may represent a useful basis for future studies to determine the impact of different antihypertensive agents on the progression of renal disease in black patients with essential hypertension.