1. Fluctuations in calcium concentrations couple myocyte depolarization with contraction and myocyte repolarization with relaxation. [1] Depolarization causes voltage sensitive calcium channels to open and calcium to flow down its concentration gradient into the myocyte. [2] This calcium current triggers the opening of calcium release channels in the sarcoplasmic reticulum and calcium pours out of the sarcoplasmic reticulum (SR). The amount of calcium released from the SR is proportional to the initial inward calcium current and to the amount of calcium stored in the SR. [3] At rest, actin–myosin interaction is prevented by troponin. When calcium binds to troponin, this inhibition is removed, actin and myosin slide relative to each other, and the cell contracts. Following contraction, calcium is actively removed from the myocyte to allow relaxation. [4] Most calcium is actively pumped into the SR where it is bound to calsequestrin. Calcium stored in the SR is thus available for release during subsequent depolarizations. The sarcoplasmic calcium ATPase is inhibited by phospholamban (Fig. 62–3). [5] The calcium sodium antiporter couples the flow of three molecules of sodium flow in one direction to that of a single molecule of calcium in the opposite direction. This transporter is passively driven by electrochemical gradients which usually favor the inward flow of sodium coupled to the extrusion of calcium. Extrusion of calcium is inhibited by high intracellular sodium or extracellular calcium concentrations and by cell depolarization. Under these conditions, the pump may “run in reverse.” [6] Some calcium is actively pumped from the cell by a calcium ATPase. [7] As myocyte calcium concentrations fall, calcium is released from troponin and the myocyte relaxes.
Source: Cardiopulmonary Medications, Goldfrank's Toxicologic Emergencies, 10e
Citation: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR. Goldfrank's Toxicologic Emergencies, 10e; 2015 Available at: Accessed: December 20, 2017
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