Abstract

The effect of 5-hydroxytryptamine (5-HT) on the isometric contraction, membrane potential, and membrane current of isolated bullfrog (Rama catesbeiana) atrium was investigated. 5-HT depressed the isometric contraction and this negative inotropism was atropine-resistant. 5-HT reduced both peak amplitude and duration of the action potential, but caused no detectable changes in the resting membrane potential and membrane input resistance. The final, or "secondary depolarization phase"1) in the rising phase of the action potential was found to be selectively depressed by 5-HT. These inhibitory effects on the action potential was also atropine-resistant. A single sucrose-gap voltage-clamp experiment revealed that 5-HT caused a reduction of the slow inward (Ca++/Na+) current. The membrane slope conductance near the resting membrane potential and the degree of activation of the of the time-dependent potassium current showed no detectable change in the presence of 5-HT. It was concluded on the basis of the present results that 5-HT directly controlled the action potential by selectively depressing the slow inward (Ca++/Na+) current. This may be responsible for the negative inotropic effect of 5-HT on bullfrog atrium.

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