Ca2+ and Ca2+-activated K+ currents in mammalian gastric smooth muscle cells.
Inward movement of calcium through voltage-dependent channels in muscle is thought to initiate the action potential and trigger contraction. Calcium-activated potassium channels carry large outward potassium currents that may be responsible for membrane repolarization. Calcium and calcium-activated potassium currents were identified in enzymatically isolated mammalian gastric myocytes. These currents were blocked by cadmium and nifedipine but were not substantially affected by diltiazem or D600. No evidence for a tetrodotoxin-sensitive sodium current or an inwardly rectifying potassium current was found.
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D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000502:physiology; D004110:Diltiazem / Q000494:pharmacology; D005711:Gallopamil / Q000494:pharmacology; D006168:Guinea Pigs; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D009130:Muscle, Smooth / Q000166:cytology / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism* / Q000502:physiology; D011817:Rabbits; D013270:Stomach / Q000166:cytology / Q000502:physiology*
D007473:Ion Channels; D002104:Cadmium; D005711:Gallopamil; D004110:Diltiazem; D009543:Nifedipine; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium