Systemic hypertension is both the cause and the consequence of renal disease. Experimental studies suggest that the adverse effects of systemic hypertension on the progression of renal disease may depend upon the intraglomerular hemodynamic consequences. Systemic hypertension accompanied by afferent arteriolar vasoconstriction is associated with normal glomerular capillary pressure and relative protection against morphologic injury. In contrast, systemic hypertension with afferent arteriolar vasodilatation leads to glomerular hypertension and is associated with structural injury. Glomerular hypertension may be present even in the setting of normal systemic pressure, as in experimental diabetes. Therapeutic interventions that attenuate glomerular capillary hypertension slow the development of glomerular injury. Dietary protein restriction, which normalizes glomerular capillary filtration, perfusion, and pressure without lowering blood pressure, retards the development of glomerular sclerosis. Alternatively, selective reduction of glomerular capillary pressure with converting-enzyme inhibitor therapy is also protective against progressive renal injury. In contrast, antihypertensive therapy, which controls systemic hypertension but does not reduce glomerular capillary pressure, fails to protect remnant kidney rats from glomerular injury. These studies suggest that control of glomerular hypertension may be of special benefit to the patient with progressive renal disease.