ICU · first-part-physiology

Cellular Physiology and Membrane Potentials — Comprehensive

Also known as Cellular physiology · Membrane potential · Action potential · Resting membrane potential · Nernst equation · Goldman-Hodgkin-Katz equation · Excitation-contraction coupling · Neuromuscular junction · Oxidative phosphorylation · Cardiac action potential phases

Cellular physiology — the biophysical basis of membrane potentials, action potentials, and excitation-contraction coupling. RESTING MEMBRANE POTENTIAL (RMP): ~-70 to -90 mV in excitable cells — generated by K+ concentration gradient (intracellular K+ 140 mmol/L, extracellular 4 mmol/L) + relative membrane impermeability to Na+ — calculated by the Goldman-Hodgkin-Katz (GHK) equation (weights each ion's contribution by its permeability). ACTION POTENTIAL (AP): in cardiac myocytes — Phase 0 (rapid depolarisation — fast Na+ influx), Phase 1 (initial repolarisation — transient K+ efflux), Phase 2 (plateau — Ca2+ influx balances K+ efflux — UNIQUE to cardiac muscle — allows sustained contraction), Phase 3 (repolarisation — K+ efflux dominates), Phase 4 (resting — Na+/K+ ATPase restores gradients). EXCITATION-CONTRACTION COUPLING: AP → voltage-gated L-type Ca2+ channel opens → Ca2+ enters → triggers ryanodine receptor → Ca2+ release from sarcoplasmic reticulum → Ca2+ binds troponin C → exposes actin binding site → myosin cross-bridge cycling → contraction. Relaxation: Ca2+ reuptake by SERCA into SR → Ca2+ dissociates from troponin → relaxation. NEUROMUSCULAR JUNCTION: motor neuron AP → voltage-gated Ca2+ channel → ACh vesicle exocytosis → ACh binds nicotinic AChR → Na+ influx → endplate potential → muscle AP. OXIDATIVE PHOSPHORYLATION: electron transport chain (complex I-IV) → proton gradient across inner mitochondrial membrane → ATP synthase → ATP from ADP + Pi.

Checked against its sources on 3 Sept 2026