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The cardiac muscle cell membrane potential is the electrical voltage difference across the cell membrane of a cardiomyocyte, which is essential for the rhythmic contraction of the heart. This potential is generated by the selective permeability of the sarcolemma to various ions, primarily sodium (Na+), potassium (K+), and calcium (Ca2+), through specialized ion channels and transporters [1]. The cardiac action potential is characterized by five distinct phases: rapid depolarization (Phase 0), brief repolarization (Phase 1), a plateau phase (Phase 2), rapid repolarization (Phase 3), and the resting membrane potential (Phase 4) [2]. Proper regulation of these phases ensures synchronized mechanical contraction, known as excitation-contraction coupling [3]. Disruptions in the membrane potential, often due to genetic mutations or drug-induced channel blockages, can lead to life-threatening arrhythmias such as ventricular tachycardia or atrial fibrillation [4]. Pharmacological intervention typically involves antiarrhythmic drugs that target the underlying ion channels to stabilize the membrane potential and restore normal sinus rhythm [5]. [1] StatPearls, Cardiac Action Potential (2023). [2] NIH, Cardiac Electrophysiology (2022). [3] CV Physiology, Cardiac Action Potential (2023). [4] PubMed, Mechanisms of Cardiac Arrhythmias (2021). [5] Goodman & Gilman's The Pharmacological Basis of Therapeutics (2018).
Modulation of voltage-gated ion channels (sodium, potassium, calcium) and ion pumps (Na+/K+-ATPase) to alter the duration, amplitude, and frequency of the cardiac action potential.
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