The electrophysiological basis of the motor inhibitory effect of adrenaline on rabbit small intestinal smooth muscle.
The spontaneous electrical activity of small intestinal smooth muscle cells consists of repetive depolarizations (control activity) on which spikes (response activity) may be superimposed; each spike is preceded by a prepotential. Response activity is associated with contractions. Adrenaline initially abolished the response activity and any prepotenials, as well as the contractions, without altering the control activity or the membrane potential. This effect was followed by hyperpolarization and slight increase in the control potential amplitude. The hyperpolarization was insenstitive tto temperature (Q10 = 1.01) and was larger when the membrane was initially depolarized by K withdrawal but did not occur after the membrane was hyperpolarized by replacing C1 by propionate or by prolonged K withdrawal. It is suggested that adrenaline inhibits intestinal motility by uncoupling the control activity to response activity through suppression of the prepotentials. The adrenaline-induced hyperpolarization may be due to an increase in K permeability but not to stimulation of electrogenic Na pumping. The increase in K permeability may depend upon the presence of Cl ions.
D000818:Animals; D002712:Chlorides / Q000502:physiology; D004594:Electrophysiology; D004837:Epinephrine / Q000494:pharmacology*; D066298:In Vitro Techniques; D007421:Intestine, Small / Q000187:drug effects*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects*; D011188:Potassium / Q000502:physiology; D011817:Rabbits; D013696:Temperature; D013997:Time Factors
D002712:Chlorides; D011188:Potassium; D004837:Epinephrine