Role of neurotransmitter release and cyclic AMP-dependent membrane phosphorylation in low voltage myocardial automaticity.
Low voltage myocardial automaticity (LVA) was investigated by pharmacological modulations of the presynaptic and postsynaptic processes. The sensitivity of LVA both to inhibitor and stimulator of neurotransmitter release suggests its involvement in LVA genesis. Moreover, LVA is blocked by the inhibition of the cyclic AMP system, supporting the participation of the c-AMP-dependent membrane phosphorylation in calcium-mediated cardiac electrogenesis.
D000328:Adult; D000526:Alprenolol / Q000494:pharmacology; D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D000242:Cyclic AMP / Q000494:pharmacology*; D004594:Electrophysiology; D006571:Heterocyclic Compounds / Q000494:pharmacology; D006801:Humans; D007097:Imines / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D010109:Oxymetazoline / Q000494:pharmacology; D010210:Papillary Muscles / Q000502:physiology*; D010766:Phosphorylation; D011817:Rabbits; D014044:Tolbutamide / Q000494:pharmacology; D014439:Tyramine / Q000494:pharmacology
D006571:Heterocyclic Compounds; D007097:Imines; D018377:Neurotransmitter Agents; C014925:RMI 12330A; D000526:Alprenolol; D010109:Oxymetazoline; D014044:Tolbutamide; D000242:Cyclic AMP; D014439:Tyramine