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

The membrane potential (Um), 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 Um, 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 Um 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.