title: Cellular mechanisms of digitalis action.
abstract: Although the therapeutic actions of digitalis glycosides have been known for over 200 years, their direct inotropic actions on the heart were not established until the last 50 years. Digitalis has undergone intense research, particularly with respect to its mechanisms of action. Many authors have claimed to have found the true mechanism of action, compounding the complexity of literature. Recent subcellular studies have pointed to specific areas of action of the digitalis glycosides. Each discovery has been dependent on the greater understanding of the electrophysiologic characteristics of cardiac muscle and excitation-contraction coupling. The current hypothesis suggests that digitalis specifically inhibits Na-K ATPase. This produces an elevation in intracellular sodium level that in turn produces an increase in the intracellular calcium level. The increased quantities of calcium available to the contractile elements of cardiac muscle provide the observed increased inotropy.
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D004071:Digitalis Glycosides / Q000494:pharmacology*; D006321:Heart / Q000502:physiology*; D006801:Humans; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D012413:Rubidium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors; D013997:Time Factors
chemical_list: D004071:Digitalis Glycosides; D010042:Ouabain; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D012413:Rubidium; D011188:Potassium; D002118:Calcium