Ionic mechanisms of intestinal electrical control activity.
The effects of inhibition and stimulation of the electrogenic Na pump and of altering the ionic environment on the electrical control activity (ECA) were studied in rabbit jejunal smooth muscle. Pump inhibition abolished the ECA at a time when the membrane potential was more negative than the peak depolarization of the control potential (CP). Pump stimulation hyperpolarized the membrane and CP's appeared. Their amplitude was initially small and progressively increased as the hyperpolarization subsided. Lowering external Na to 20 mM or Ca withdrawal, but not addition of verapamil, reversibly abolished the ECA. Chloride replacement by propionate, isethionate, or benzene-sulphonate caused a transient augmentation, followed by suppression of the secondary depolarization of the CP's and decreased their frequency. The initial depolarization of the CP was little affected. Nitrate substitution increased CP frequency and spiking activity but had no observable effects on the CP configuration. These results suggest that the intestinal control potential may result from conductance changes initially to Na and later to C1 rather than fron an oscillatory electrogenic pump.
D000818:Animals; D001557:Benzenesulfonates / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology; D004594:Electrophysiology; D066298:In Vitro Techniques; D007513:Isethionic Acid / Q000494:pharmacology; D007583:Jejunum / Q000378:metabolism / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D009130:Muscle, Smooth / Q000378:metabolism / Q000502:physiology*; D011422:Propionates / Q000494:pharmacology; D011817:Rabbits; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
D001557:Benzenesulfonates; D011422:Propionates; D007513:Isethionic Acid; D012964:Sodium; D014700:Verapamil; D002118:Calcium