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

1 Bay K 8644 (0.33 n m to 1 μ m ) greatly increased the contractions of rat urinary bladder detrusor muscle induced by β,γ‐methylene ATP (β,γ‐MeATP, 10 μ m ) and by electrical field stimulation of the purinergic component (the cholinergic response was blocked by atropine). 2 The contractions induced by acetylcholine (ACh, 10 μ m ) 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 n m to 3.3 μ m ) 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 n m ). At concentrations greater than 1 μ m , Bay K 8644 inhibited contraction. 5 It is concluded that voltage‐sensitive calcium channels play an important role in the excitatory mechanical action of P 2x ‐purinoceptor‐mediated purinergic responses in the rat urinary bladder, while cholinergic‐mediated responses are less dependent on such channels.