Calcium and Cardiac Electrophysiology

Some Experimental Considerations

¹ From the Department of Physiology, University of Pennsylvania School of Medicine, Philadelphia

Electrophysiologic experiments in cardiac tissue suggest that Ca²⁺ is involved in generation of the action potential, the pacemaker potential, and conduction of the slow wave of depolarization. For instance, removal of Ca²⁺ inhibits the slow inward current and prolongs the action potential and suppresses the slow diastolic depolarization. Divalant cations Mn²⁺, Co²⁺, Cd²⁺, Mg²⁺, block the slow inward current and suppress pacemaker activity, but shorten the action potential. Ni²⁺ specifically blocks the slow inward current and prolongs the action potential. Ca²⁺ also plays a central role in generation of diastolic depolarization. Cd²⁺ inhibits the diastolic depolarization and the upstoke of the action potential in SA nodal cells, while blocking the time-dependent inward current in the pacemaker potential range and the time-dependent outward current. A variety of molecular transport systems ranging from the Ca-channel to a (Ca²⁺-Na⁺ or Ca²⁺-K⁺ exchanges to Ca²⁺-induced activation of the K⁺ current have been postulated to explain the effects of Ca²⁺ on cardiac electrophysiologic processes.