The Na+ -K+ -activated ATPase is required to maintain osmotic balance and stabilize cell volume. The Na+ -K+ -ATPase has a more direct role in regulating cell volume; it controls the solute concentrations inside the cell, thereby regulating the osmotic forces that can make a cell swell or shrink. The impotance of the Na+ -K+ -ATPase in controlling cell volume is indicated by the observation that animal cells swell, and may burst, if they are treated with ouabain, which, inhibits the Na+ -K+ -ATPase. The present experiment was designed and carried out to determine the effect of verapamil, a calcium blocker, on the activity of Na+ -K+ -ATPase prepared from renal medulla in the normal rabbit. It was reported that verapamil, a well known coronary vasodilator, possessed negative inotropic effects. The mechanism of action of verapamil was initially thought to be due to coronary vasodilation and blockade of myocardial B-adrenergic receptors. 1t was termed such agent calcium antagonist. A derivative of verapamil, D-600, was subsequently shown to block the movement of calcium through the slow channel and thereby after the plateau phase of the cardiac action potential. Verapamil do not directly antagonize the effects of calcium. Rather, it inhibit the entry of ealcium into cells or its mobilization form intracellular stores and, as such, have been termed a calcium channel blocker.
Action Potentials ; Adenosine Triphosphatases* ; Adenosine* ; Animals ; Calcium ; Calcium Channels ; Cell Size ; Gallopamil ; Ouabain ; Vasodilation ; Verapamil*