The effects of Bay K 8644 and nifedipine on the responses of rat urinary bladder to electrical field stimulation, β,γ‐methylene ATP and acetylcholine

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Abstract
1 Bay K 8644 (0.33 nm to 1 μm) greatly increased the contractions of rat urinary bladder detrusor muscle induced by β,γ-methylene ATP (β,γ-MeATP, 10 μm) and by electrical field stimulation of the purinergic component (the cholinergic response was blocked by atropine). 2 The contractions induced by acetylcholine (ACh, 10 μm) and by electrical field stimulation of the cholinergic component (the purinergic response was blocked following desensitization by α,β-MeATP) were also potentiated by Bay K 8644, although to a lesser extent than the purinergic responses. 3 Nifedipine (1 nm to 3.3 μm) inhibited all the contractions induced by β,γ-MeATP, ACh and electrical field stimulation. However, while the responses to β,γ-MeATP and electrical field stimulation of the purinergic component were almost abolished, a substantial proportion of the responses to ACh and electrical field stimulation of the cholinergic component were nifedipine resistant. 4 The concentration-effect curves for the potentiation by Bay K 8644 of the responses to β,γ-MeATP, ACh and electrical field stimulation were shifted to the right by nifedipine (10 nm). At concentrations greater than 1 μm, Bay K 8644 inhibited contraction. 5 It is concluded that voltage-sensitive calcium channels play an important role in the excitatory mechanical action of P2x-purinoceptor-mediated purinergic responses in the rat urinary bladder, while cholinergic-mediated responses are less dependent on such channels.