Key Points
- To examine how transient changes in external sodium concentration generate membrane currents mediated by sodium-calcium exchange in cesium-loaded frog heart cells.
- Applied voltage-clamp protocols to isolated frog heart cells preloaded with cesium, using tetrodotoxin and cesium to block endogenous sodium and potassium currents.
- Measured membrane currents evoked by transiently lowering external sodium to 39.2 mM and subsequently restoring standard sodium concentrations across various membrane potentials.
- Assessed current modulation by varying external calcium, manipulating intracellular pH with 10 mM NH4Cl, and applying diverse pharmacological blockers.
- Reducing external sodium generated a U-shaped outward current across depolarizing and hyperpolarizing potentials, whereas restoring standard sodium evoked a bell-shaped inward current.
- Current amplitude scaled with external calcium concentration, increased with intracellular alkalinization via 10 mM NH4Cl, and markedly decreased with intracellular acidification.
- The current was inhibited by La3+, Co2+, D600, adriamycin, quinidine, and disopyramide, but was unaffected by lidocaine or nifedipine.
Structured PICO
PPopulationFrog heart cells previously loaded with Cs
IInterventionTransient alterations in external sodium (Nao) (application of Na-poor solution 39.2 mM followed by standard solution)
CComparatorStandard solution / baseline conditions
OOutcomeMembrane current generation (outward and inward currents) related to Na-Ca exchangesurrogate
This preclinical study demonstrates that Na-Ca exchange in frog heart cells generates a measurable membrane current that is outward during calcium influx.