title: Inhibition of sodium-dependent calcium overload to treat myocardial ischemia.
abstract: Because intracellular sodium and calcium overload play a key role in both mechanical and electrical dysfunction during myocardial ischemia, inhibition of the late sodium current would be expected to decrease the intracellular sodium and calcium overloads and thereby reduce their undesirable effects. Ranolazine selectively inhibits late sodium current relative to peak sodium current, and attenuates the abnormalities of ventricular repolarization and contractility associated with ischemia. This is the currently proposed mechanism (hypothesis) of action of the effects of ranolazine during myocardial ischemia.
authors.forename: C R
authors.initials: CR
authors.lastname: Conti
mesh_terms: D000083:Acetanilides; D000787:Angina Pectoris / Q000188:drug therapy*; D004791:Enzyme Inhibitors / Q000627:therapeutic use*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D017202:Myocardial Ischemia / Q000188:drug therapy*; D010879:Piperazines / Q000627:therapeutic use*; D000069458:Ranolazine; D026941:Sodium Channel Blockers / Q000627:therapeutic use*; D019831:Sodium-Calcium Exchanger / Q000502:physiology*
chemical_list: D000083:Acetanilides; D004791:Enzyme Inhibitors; D010879:Piperazines; D026941:Sodium Channel Blockers; D019831:Sodium-Calcium Exchanger; D000069458:Ranolazine