An evidence for presynaptic excitatory alpha₂-adrenergic receptors in frog myocardium

Y. Sarioglu Cumhuriyet University, Faculty of Medicine, Department of Pharmacology, Sivas and Hacettepe University, Faculty of Medicine, Department of Pharmacology, Ankara, Turkey

M. Ilhan Cumhuriyet University, Faculty of Medicine, Department of Pharmacology, Sivas and Hacettepe University, Faculty of Medicine, Department of Pharmacology, Ankara, Turkey; Department of Pharmacology, Faculty of Medicine, Hacettepe University, Ankara, Turkey

S. O. Kayaalp Cumhuriyet University, Faculty of Medicine, Department of Pharmacology, Sivas and Hacettepe University, Faculty of Medicine, Department of Pharmacology, Ankara, Turkey

Abstract

This study was undertaken to determine the effects of clonidine on sympathetic neurotransmission in frog myocardium. In the electrically driven ventricular strips of frog heart, clonidine was found to be ineffective on contractility. However, clonidine increased the positive inotropic responses to transient additional stimulations. This effect of clonidine was antagonized by yohimbine, an α₂-adrenergic receptor antagonist. Clonidine did not change the positive inotropic effects of exogenously applied noradrenaline. These results suggest that clonidine facilitates sympathetic neurotransmission in frog myocardium via an action on α₂-adrenergic receptors located on sympathetic nerve terminals.

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An evidence for presynaptic excitatory alpha₂-adrenergic receptors in frog myocardium

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An evidence for presynaptic excitatory alpha₂-adrenergic receptors in frog myocardium