This preclinical study aimed to investigate the effects of catecholamine-related drugs on atrial responses to cholinergic stimulation in isolated guinea-pig atria.
No immediate clinical implications; leaves open autonomic drug interactions in atrial tissue for further study.
Hukovic (1) was the first to suggest the existence of the cholinergic fibers in the sympathetic nerve of the rabbit's atria. He showed that stimulation of the sympathetic nerve in the isolated reserpinized heart produced the negative chrono and inotropic effects which were potentiated by eserine and abolished by atropine. A series of experiments in this laboratory (2-5) have excluded an essential role of the heart catecholamine on initiation and maintenance of the spontaneous contraction and action potential of the rabbit's atria. Recently, Misu (6, 7) and Misu and Takaori (8) in this laboratory have demonstrated that the atrial action potentials abolished by the concentration of 10-5 of dibenarnine, chlorpromazine and yohimbine, are restarted by adrenaline as well as by acetylcholine, and that noradrenaline mainly shortens the repolarization phase of the potential, while acetylcholine serves to restore the depolarization phase. This suggests a modulating role of the endogenous noradrenaline in the rhythmic contraction or action potential of the heart, and led us to study the effects of catecholamine-relating drugs on the atrial responses to cholinergic stimulation.
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Toda et al. (1964) studied this question.
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