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Mechanisms of excitatory neuromuscular transmission in the guinea‐pig urinary bladder

1 In smooth muscle of the guinea‐pig bladder, either membrane potential recordings or [Ca2+]i measurements were made simultaneously with isometric tension recordings. 2 Single transmural stimuli initiated excitatory junction potentials (EJPs) which triggered action potentials, transient increases in [Ca2+]i and associated contractions. These responses were abolished by α,β‐methylene ATP, suggesting that they resulted from the activation of purinoceptors by neurally released ATP. 3 Nifedipine abolished action potentials leaving the underlying EJPs and reduced the amplitude of both nerve‐evoked increases in [Ca2+]i and associated contractions. The subsequent co‐application of caffeine and ryanodine inhibited the residual responses without inhibiting EJPs. These results indicate that stimulation of purinoceptors activates both Ca2+ influx through L‐type Ca2+ channels and Ca2+ release from intracellular Ca2+ stores. 4 In the presence of α,β‐methylene ATP, trains of stimuli failed to initiate EJPs but increased the frequency of action potentials. Trains of stimuli also initiated oscillatory increases in [Ca2+]i and associated contractions. These responses were abolished by hyoscine, indicating that they resulted from the activation of muscarinic receptors by neurally released ACh. 5 Oscillatory increases in [Ca2+]i and associated contractions were inhibited by either nifedipine or caffeine, indicating that the stimulation of muscarinic receptors activates both Ca2+ influx through L‐type Ca2+ channels and Ca2+ release from intracellular Ca2+ stores.