Key Points
- To determine the electrophysiological effects of the dihydropyridine calcium channel blocker nitrendipine on sodium currents in cultured neonatal rat ventricular myocytes.
- Measured whole-cell currents in single cultured neonatal rat ventricular cells using the patch-clamp technique.
- Isolated sodium currents by eliminating potassium currents (internal/external cesium, TEA, 4-aminopyridine) and blocking calcium currents with external cobalt.
- Nitrendipine caused a dose-dependent reduction of sodium currents with a half-maximum inhibitory concentration of 3 × 10⁻⁶ M at a holding potential of -80 mV.
- Nitrendipine shifted the steady-state inactivation curve to hyperpolarized potentials, enhanced blockade at pulse intervals shorter than 1000 ms, and prolonged repriming kinetics similarly to lidocaine.
- The sodium channel blockade was reversed in the presence of the dihydropyridine agonist Bay K8644.
Structured PICO
PPopulationSingle cultured ventricular cells from neonatal rats
OOutcomeSodium current amplitude and kineticssurrogate
The calcium channel blocker nitrendipine also exhibits dose-dependent sodium channel blocking effects in cardiac myocytes, similar to local anesthetics like lidocaine.