Calcium entry blockers exert several characteristic effects on renal function that contribute to their blood-pressure lowering capacity. They are able to dilate renal vasculature and, in certain circumstances, can increase the glomerular filtration rate, both effects being dependent on the preexisting vascular tone. Calcium blockers are also able to increase renal sodium excretion, mainly through a direct tubular effect that remains during the chronic administration of these drugs. These effects clearly differentiate calcium entry blockers from nonspecific vasodilators and contribute to their effectiveness when they are used as first-step drugs in the therapy of arterial hypertension.