Cardiac myocyte membrane potential (null)

The cardiac myocyte membrane potential refers to the difference in electrical charge across the plasma membrane of heart muscle cells. This transmembrane voltage arises from selective permeability to ions—primarily sodium (Na+), potassium (K+), and calcium (Ca2+)—through specialized protein channels. At rest, ventricular myocytes typically have a stable negative resting membrane potential around -90 mV due mainly to high K+ conductance[3]. Upon stimulation by an action potential from neighboring cells via gap junctions, rapid opening and closing sequences among different voltage-gated Na+, Ca2+, and K+ channels generate characteristic phases—depolarization (phase 0), initial repolarization (phase 1), plateau phase due to Ca2+ influx balanced by K+ efflux (phase 2), rapid repolarization (phase 3), and return to resting state (phase 4)[5][7]. These dynamic changes underlie coordinated contraction necessary for effective pumping function. Many antiarrhythmic agents act on these underlying ionic currents by blocking specific types of ion channels; thus while “cardiac myocyte membrane potential” itself is not a druggable target per se, its regulation is central both physiologically and therapeutically[2]. "Cardiac myocyte membrane potential" describes an essential physiological process governed by multiple molecular entities rather than being itself a canonical drug target. For structured data purposes regarding therapeutic intervention or mechanistic studies, focus should shift toward individual cardiac ion channels such as Nav1.5 sodium channel (SCN5A gene product), L-type calcium channel (CACNA1C gene product), etc.[6]

Other names

Cardiac action potentialMyocardial cell membrane potentialCardiomyocyte resting potential

Mechanisms relate to modulation of underlying ion currents via specific molecular targets: Blockade or enhancement of sodium current (I_Na), blockade or enhancement of potassium current (I_K), and blockade or enhancement of calcium current (I_Ca).