(0.33 nm to 1 pM) greatly increased the contractions of rat urinary bladder detrusor muscle induced by fI,y-methylene ATP (f,y-MeATP, 10pMm) and by electrical field stimulation of the purinergic component (the cholinergic response was blocked by atropine). 2 The contractions induced by acetylcholine (ACh, 10PM) and by electrical field stimulation of the cholinergic component (the purinergic response was blocked following desensitization by a,/8-MeATP) were also potentiated by Bay K 8644, although to a lesser extent than the purinergic responses.3 Nifedipine (1 nm to 3.3jpM) inhibited all the contractions induced by /iy-MeATP, ACh and electrical field stimulation. However, while the responses to fly-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 fl,y-MeATP, ACh and electrical field stimulation were shifted to the right by nifedipine (10 nM). At concentrations greater than 1 pM, Bay K 8644 inhibited contraction. 5 It is concluded that voltage-sensitive calcium channels play an important role in the excitatory mechanical action of P21-purinoceptor-mediated purinergic responses in the rat urinary bladder, while cholinergic-mediated responses are less dependent on such channels.