Calcium channels, potassium channels and membrane potential of smooth muscle cells of human allantochorial placental vessels

The membrane potential (U_m), the main factor of the excitation–contraction coupling, of human allantochorial placental vascular smooth muscle cells (VSMCs) has been previously shown to depend on voltage-sensitive K⁺ channels. These channels were blocked by high external K⁺. To characterize other channels which regulated U_m, various constrictor or/and vasodilators and channel blockers were used. Serotonin depolarized VSMCs, in normal medium, but induced a more marked depolarization in VSMCs predepolarized by high external K⁺. This depolarization was inhibited by nifedipine, a blocker of voltage-gated Ca²⁺ channels. Acetylcholine, sodium nitroprusside (without effect on U_m in normal medium), hyperpolarized the predepolarized-high K⁺ medium VSMCs. This hyperpolarization was inhibited after addition of charybotoxin (a blocker of Ca²⁺-activated K⁺ channels) or/and glibenclamide (a blocker of ATP-sensitive K⁺ channels). A similar effect was obtained with isoproterenol. These results indicated that membrane potential of human placental allantochorial VSMCs was regulated by voltage-gated, Ca²⁺- and ATP-sensitive K⁺ channels and by voltage-dependent Ca²⁺ channels.