Role of nicotinic acetylcholine receptor subtypes on nicotine’s enhancing effect on electrical field stimulation elicited contractile responses in rabbit urine bladder

摘要

OBJECTIVE: This study aims to investigate the contribution of presynaptic nicotinic acetylcholine receptors (nAChRs) sub-types to nicotine-induced enhancement in electrical field stimulation (EFS) EFS-mediated contractile responses in rabbit urine bladder smooth muscle preparations. MATERIALS AND METHODS: Rabbit urine bladder smooth muscle strips were placed in organ baths containing 20 ml of an aerated Krebs-Henseleit solution, and contractions were recorded using isometric force displacement transducers. Following the acquisition of control EFS (60 V, 8 Hz, 1 ms) responses, nicotine was added to the bath at a 3×10-5 M concentration, and EFS responses were obtained. The effect of nAChR antagonists on nicotine-induced augmentation in EFS-mediated responses was investigated in the presence of hexamethonium, dihydro-β-erythroidine, mecamylamine, and α-bungarotoxin. RESULTS: Tetrodotoxin (TTX; 10-6 M) completely blocked EFS-induced contractile responses in smooth muscle strips. Similarly, Atropine (10-6 M), when administered with α,β-methylene adenosine triphosphate (α,β-methylene-ATP) (10-5 M), completely blocked EFS responses. Nicotine significantly enhanced EFS-mediated contractile responses (23.67% ± 1.75). Nicotine-induced increases in EFS responses were largely inhibited by hexamethonium, mecamylamine, and dihydro-β-erythroidine, whereas α-bungarotoxin only partly inhibited these enhancements. CONCLUSIONS: These findings demonstrate that EFS-induced neurogenic contractions in rabbit urine bladder smooth muscle strips are mediated by purinergic and cholinergic transmissions, and the α4β2, α3β4, and α7 sub-types of nAChRs contribute to the enhancement effect of nicotine on EFS-induced contractile responses.