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

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.