The effect of nitric oxide on acetylcholine release in the rabbit bladder.

Abstract We evaluated the effects of nitric oxide (NO) on acetylcholine release and the contractile response induced by electrical field stimulation in rabbit bladder smooth muscles using a muscle bath and high performance liquid chromatography coupled with microdialysis. Electrical field stimulation (supramaximum voltage, pulse duration 0.5 ms, frequency 5 and 20 Hz) was applied to a smooth muscle strip isolated from rabbit bladder. With low-frequency (5 Hz) stimulation, pretreatment with N ω -nitro- l -arginine ( l -NNA) (100 μM) significantly increased electrical field stimulation-induced acetylcholine release and contractile response, which were reduced by the addition of l -arginine. Pretreatment with sodium nitroprusside in the absence or presence of l -NNA significantly decreased electrical field stimulation-induced acetylcholine release and contractile response. In contrast, with high frequency (20 Hz) stimulation, pretreatment with l -NNA and sodium nitroprusside had no significant effect on either contractile response or acetylcholine release. Pretreatment with sodium nitroprusside caused no significant changes in carbachol and ATP-induced contractile responses. Sodium nitroprusside and l -NNA had no significant effects on the atropine-resistant part of the contraction induced by electrical field stimulation in rabbit bladder smooth muscles. The results suggest that there is a NO-mediated mechanism inhibiting acetylcholine release from cholinergic nerve endings in rabbit bladder, which may contribute to bladder function.