High resting adenylate cyclase activity, implying a high basal adenosi
ne 3',5'-cyclic monophosphate level, seems to be a distinctive propert
y of sinoatrial node cells of mammalian heart. This may explain why ac
etylcholine depresses two ionic mechanisms involved in spontaneous act
ivity of nodal myocytes, via inhibition of adenylate cyclase activity,
without previous beta-adrenergic stimulation.