Cell membrane Na+, K+-ATPase and sarcoplasmic reticulum: possible regulators of intracellular ion activity

Abstract

Cardiac muscle requires an external source of calcium for contraction, but current evidence supports an intracellular pool of bound calcium as the primary activator of contraction. The size of this intracellular pool modulates the amount of calcium released to troponin during systole and the resultant contractile response. Proposed mechanisms for modulation of activator calcium include: 1) an alteration in phase II "slow current" allowing increased electrogenic calcium flux; 2) a glycoside independent sodium-calcium exchange across the sarcolemma that can be modulated by changes in the sodium gradient; 3) potassium-calcium exchange system during cardiac repolarization; 4) an augmentation of calcium accumulation by cardiac sarcoplasmic reticulum related to various phosphorylation mechanisms; and 5) an alteration in phospholipid affinity effected by cardiac glycoside at sarcolemmal sites related to the Na+, K+-ATPase.