Key result
Voltage clamp experiments in ventricular myocytes showed the total charge carried by the nifedipine-sensitive inward calcium current is twice the charge carried by the sodium-calcium exchange current.
In ventricular myocytes, all calcium entering the cell during initial depolarization is extruded by the sodium-calcium exchange, assuming a 3:1 sodium to calcium stoichiometry.
Reinforces NCX as sole calcium extruder in myocytes under 3:1 stoichiometry; leaves open translation to human ventricular function.
Ventricular myocytes exhibit a nifedipine-sensitive inward calcium current (ICa) and contracture when they are voltage clamped from -40 to 0 millivolt in the presence of caffeine and in the absence of extracellular sodium. However, upon repolarization they fail to relax because neither the sarcoplasmic reticulum nor the sodium-calcium exchange can reduce intracellular calcium. Sudden application of extracellular sodium during the contracture (but after repolarization) causes immediate relaxation and activates a transient inward sodium-calcium exchange current (INa-Ca), whose peak slightly precedes mechanical relaxation. The total charge carried by the nifedipine-sensitive ICa is twice the total charge carried by the transient inward INa-Ca. Assuming an exchange stoichiometry of three sodium to one calcium, these results indicate that all the calcium entering the cell during the initial depolarization is extruded by the sodium-calcium exchange.
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Bridge et al. (1990) studied Cardiac myocytes. Extracellular sodium application was evaluated on Relationship between charge movements of ICa and INa-Ca. Voltage clamp experiments in ventricular myocytes showed the total charge carried by the nifedipine-sensitive inward calcium current is twice the charge carried by the sodium-calcium exchange current.
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