title: 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 Nomega-nitro-L-arginine (L-NNA) (100 microM) 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.
authors.affiliation: Department of Urology, Kumamoto University School of Medicine, Honjo, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Miyamoto
authors.forename: M
authors.initials: M
authors.lastname: Yoshida
authors.forename: W
authors.initials: W
authors.lastname: Takahashi
authors.forename: A
authors.initials: A
authors.lastname: Inadome
authors.forename: M
authors.initials: M
authors.lastname: Yono
authors.forename: H
authors.initials: H
authors.lastname: Seshita
authors.forename: S
authors.initials: S
authors.lastname: Murakami
authors.forename: S
authors.initials: S
authors.lastname: Ueda
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D017551:Microdialysis; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011817:Rabbits; D001743:Urinary Bladder / Q000187:drug effects / Q000378:metabolism*; D014665:Vasodilator Agents / Q000494:pharmacology; D019323:omega-N-Methylarginine / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D018727:Muscarinic Antagonists; D014665:Vasodilator Agents; D009599:Nitroprusside; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D011189:Potassium Chloride; D001285:Atropine; D001120:Arginine; D019001:Nitric Oxide Synthase; D000109:Acetylcholine