Abstract

(1) The double sucrose-gap method was used to record changes in membrane resistance in intestinal smooth muscle strips. (2) Adrenaline reduced the membrane resistance; it hyperpolarized the membrane and blocked spontaneous and evoked spikes. (3) When the membrane potential was shifted by applying conditioning current, the hyperpolarization produced by adrenaline was larger during depolarization and smaller during hyperpolarization. The hyperpolarization caused by adrenaline was converted into depolarization by 18 to 20 mV conditioning hyperpolarization. (4) The resting membrane resistance was increased in the absence of potassium and in low external chloride (replaced with benzene- or ethane-sulphonate); it was decreased by excess potassium and by nitrate substitution for chloride. (5) The reduction of the membrane resistance by adrenaline was potentiated by high external potassium and by replacement of chloride with nitrate; it was diminished by low external potassium and by replacement of chloride with benzene- or ethane-sulphonate. (6) The hyperpolarization by adrenaline was reduced by raising the external potassium concentration; it was increased by lowering the external potassium concentration. In a solution containing low chloride and high potassium (24 m M ), adrenaline often produced depolarization. (7) It was concluded that adrenaline increases mainly the potassium conductance and also the chloride conductance of the smooth muscle cell membrane. Sodium seemed to be less important for the adrenaline action.

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