Substantial evidence indicates that the adverse effects of hypertension on the kidney depend on the degree to which systemic blood pressure elevations are transmitted to the renal microvasculature. Such blood pressure transmission and consequent susceptibility to hypertensive renal damage is markedly exacerbated in states characterized by preglomerular vasodilation and an impairment of the normally protective renal autoregulatory mechanisms, e.g. diabetes or chronic renal disease. Moreover, this pathophysiology gives rise to the prediction that prevention of hypertension-induced barotrauma will require blood pressure to be reduced well into the normotensive range in such patients, as is being recognized in the currently recommended blood pressure goals. Agents that block the renin-angiotensin system should be preferred as initial therapy as they may provide additional risk reductions and minimize the potassium and magnesium depletion associated with the diuretic use usually necessary to achieve the lower blood pressure targets. The current failure to achieve optimal blood pressure reductions may be contributing not only to the still escalating incidence of end-stage renal disease in diabetic patients, but also to their greatly increased cardiovascular morbidity and mortality.