Sodium-calcium exchange in mammalian heart: current-voltage relation and intracellular calcium concentration

• Published in: Molecular and cellular biochemistry 1989-09, Vol.89 (2), p.97-102
• Main Authors: Wier, W G, Beuckelmann, D J
• Format: Article
• Language: English
• Subjects: Animals; Benzofurans; Calcium - metabolism; Calcium Channels; Carrier Proteins - metabolism; Cesium - pharmacology; Electrophysiology; Fluorescent Dyes - analysis; Fura-2; Guinea Pigs; Ion Exchange; Membrane Potentials; Myocardium - metabolism; Nickel - pharmacology; Perfusion; Ryanodine - pharmacology; Sodium - metabolism; Sodium-Calcium Exchanger; Tetrodotoxin - pharmacology; Verapamil - pharmacology
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/BF00220759

Membrane currents and changes in intracellular calcium ion concentration ([Ca2+]i) have been recorded that can be attributed to the operation of an electrogenic, voltage-dependent sodium-calcium (Na-Ca) exchanger in mammalian heart cells. Single guinea-pig ventricular myocytes under voltage clamp were perfused internally with the fluorescent Ca2+-indicator, fura-2, and changes in [Ca2+]i and membrane current that resulted from Na-Ca exchange were isolated through the use of various organic channel blockers (verapamil, TTX), impermeant ions (Cs+, Ni2+), and inhibitors of sarcoplasmic reticulum (ryanodine). The I-V relation of Na-Ca exchange was obtained from the Ni2+-sensitive current elicited by ramp repolarization from +90 mV to -80 mV. Ramps were sufficiently rapid that little change in [Ca2+]i occurred during the ramp. The (constant) [Ca2+]i during the ramp was varied over the range 100 nM to 1000 nM by varying the amplitude and duration of a pre-pulse to the ramp. The reversal potential of the Ni2+-sensitive ramp current varied linearly with 1n[( Ca2+])i. The I-V relations at different [Ca2+]i over the range -60 mV to +140 mV were in reasonable accord with the predictions of a simple, simultaneous scheme of Na-Ca exchange, on the basis that only [Ca2+]i had changed. The relationship between [Ca2+]i and current at a constant membrane voltage was also in accord with this scheme. We suggest that Ca2+-fluxes through the exchanger during the cardiac action potential can be understood quantitatively by considering the binding of Ca2+ to the exchanger during the [Ca2+]i-transient and the effects of membrane voltage on the exchanger.