Key result
Clonidine increased positive inotropic responses in frog myocardium, suggesting it facilitates sympathetic neurotransmission via presynaptic alpha2-adrenergic receptors.
No clinical implications for inotrope therapy; leaves open presynaptic alpha2 facilitation of sympathetic transmission in mammalian myocardium.
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 alpha 2-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 alpha 2-adrenergic receptors located on sympathetic nerve terminals.
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Sarıoğlu et al. (1988) studied this question. Clonidine was evaluated on Positive inotropic responses to transient additional stimulations. Clonidine increased positive inotropic responses in frog myocardium, suggesting it facilitates sympathetic neurotransmission via presynaptic alpha2-adrenergic receptors.
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