In addition to factors such as protein intake or hyperlipidemia, hypertension contributes to the progressive deterioration of renal function in experimental animal models of renal disease, and has a prominent role in the imbalance of intrarenal hemodynamics. Reduction of arterial pressure was shown to alter the course of human chronic renal disease. In patients with diabetic as well as nondiabetic nephropathy, the lowering of proteinuria by angiotensin-converting enzyme inhibitors is greater than that observed with other antihypertensive drugs and appears to be independent of blood pressure control alone, whereas albuminuria may be unaffected or worsened during nifedipine treatment. Angiotensin-converting enzyme inhibitors may afford better protection than conventional treatment at various stages of diabetic nephropathy and prevent the evolution from incipient to overt nephropathy. In patients with nondiabetic renal disease, no unequivocal evidence exists for such a protective effect. In renal transplant recipients receiving cyclosporine, converting enzyme inhibitors and calcium antagonists are equally effective in the control of hypertension and both leave unaltered the glomerular filtration rate. It remains to be demonstrated, using adequate study designs, whether a particular class of agent is superior to another in patients with chronic renal disease.