Cardiac myocyte, contraction, action potential conduction, action potential for non-pacemaker cells, pacemaker, electrocardiography

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Biomedical Science
BMS 420
Charles Miller

19 September 28 MC 2 short answer Cardiac Myocyte Sliding filament mechanism T tubules extend from sarcolemma and permit extracellular ions and fluid to diffuse near intracellular structures Sarcoplasmic reticulum stores substantial amounts of Ca which is released when ++ ryanodine receptors are stimulated by extracellular Ca which flow through L type voltage sensitive dihydropyridine receptors Calcium induced calcium release Ryanodine receptors – activated by calcium, initiate calcium release Intercalated discs allow low resistance for charge to flow from cell to cell ++ ++ Ca enters cytoplasm via VG L-type Ca channels which interact with ryanodine receptors on SPR (“trigger calcium”). Calcium induced calcium release. ++ ++ Ca released from sequestered Ca Tropomyosin is associated with three regulatory proteins: TN-T, TN-C, and TN-I Ca binds to TN-C which in presence of ATP changes conformation of troponin Myosin and actin cross-bridge when myosin binding sites exposed on actin SERCA-resequesters Ca via phosphorylation of phospholamban (SERCA = SPEndoreticulum CaATPase) Calsequestrin is the primary calcium storage protein in the SR. It binds to approximately 50 Ca + + ++ ions per molecule during diastole which prevents Ca precipitation. ++ Ca releases from TN-C and inhibition of binding sites occurs → relaxation ATP needed for contraction and relaxation (lusitropy) Conduction Pathways SA node → atrial muscle → AV node → bundle of His → right and left bundle branches → Purkinje fibers → ventricular muscle Delay at AV node Most of end-diastolic volume reaches the ventricles due to the pressure difference rather than atrial contraction SA node generates fastest signal (60/min) Generation gets slower farther down the chain SA node, while functional, overrides the others SA node does not have resting membrane potential Action Potential Conduction IAB= (V A V )B/ R AB IAB– current between cells A and B V – voltage R – resistance Depolarizing current or + charges Current flows from depolarized to hyperpolarized within cell Ion causing rapid upswing of action potential Ventricular muscle – sodium SA node – calcium Action Potential for Non-pacemaker Cells Phase 0: Depolarization phase + + Opening of fast Na channels with fall in K leakage out + Site for antiarrhythmic drugs (block Na channels) ERP: Na inactivated; RRP: Na channels closed. Phase
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