The normal kidney can increase its rate of glomerular filtration in response to an acute protein load. It has been suggested that this acute hyperfiltration represents a renal functional reserve (RFR). The RFR has also been proposed to reflect the chronic hyperfiltration found in diabetic patients and animal models of chronic renal failure. The physiologic role of the RFR is still unclear. On the one hand, the availability of an RFR may retard the progression towards end-stage renal failure. On the other hand, sustained hyperfiltration has been implicated as a potential deleterious factor in the progression of renal disease. Antihypertensive drugs used in the management of hypertensive patients with chronic renal disease modify both the systemic and the renal hemodynamics. Depending on their hemodynamic effects, they may thereby alter the ability to mobilize RFR. Today, it is still not clear whether an ideal compound should increase, decrease, or not affect RFR to preserve long-term renal function. Evaluation of the effects of various antihypertensive agents on RFR could become an important aspect of consideration in order to optimize both the control of blood pressure and the capacity of the therapy to prevent deterioration of renal function.