The relationships between systemic arterial pressures, renal blood flow, filtration, and sodium homeostasis are complex. Considerable evidence has accrued indicating that changes in renal sodium handling as a function of perfusion pressure participate in the pathogenesis of hypertension. Central to this viewpoint is the normalization of BP after transplantation of a normal kidney to a hypertensive host, both in animals and humans. Renal blood flow varies inversely with the severity and duration of hypertension. Studies of regional hemodynamics underscore the importance of independent regulation of different vascular beds. Some observations suggest that abnormal renal vascular reactivity may be among the earliest changes in essential hypertension. The degree to which these represent structural changes as opposed to functional responses to endocrine or neurogenic stimuli may vary under different circumstances and merits further study. Although antihypertensive therapy generally has been well tolerated by the kidney, deterioration of renal function has been encountered during pharmacological BP reduction. In the presence of preglomerular arterial disease, blood flow and filtration may become sensitive to hemodynamic fluctuations, which leads to the designation of "critical perfusion pressure." Awareness of the mechanisms by which changes in systemic hemodynamics impinge upon renal function may lead to more rational use of specific antihypertensive agents.