Data from several studies have indicated that calcium channel blockers may prevent acute renal damage caused by ischemia. If this is true, then the obvious clinical application of this premise would be in surgical cases requiring cross-clamping of the aorta, or in patients experiencing prolonged hypotension. Evidence for the mechanism by which calcium channel blockers mitigate injury include the prevention or amelioration of renal vasoconstriction and/or their ability to inhibit calcium entry into cells, thereby possibly preventing toxic calcium ‘overload’. Studies of animal models examining ischemic acute renal failure produced either by infusion of vasoconstrictors or by interrupting renal artery blood flow have provided conflicting results. Certain calcium channel blockers afford some degree of protection only when administered prior to the ischemic episode, while others may protect even if given after the insult. Several investigations have been carried out to determine the mechnism(s) of this protective effect. The results indicate cellular calcium accumulation occurs in cells during the anoxic period; this is most pronounced during reflow. This accumulation of calcium appears to be temporally related to both mitochondrial dysfunction and cell death. The ability of the calcium channel blockers to prevent calcium entry into cells may explain their role in protecting the cell and ameliorating ischemic inj