Abstract
High resting adenylate cyclase activity, implying a high basal adenosine 3', 5'-cyclic monophosphate level, seems to be a distinctive property of sinoatrial node cells of mammalian heart. This may explain why acetylcholine depresses two ionic mechanisms involved in spontaneous activity of nodal myocytes, via inhibition of adenylate cyclase activity, without previous b-adrenergic stimulation.
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