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

Abstract

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 3x10(-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-beta-erythroidine, mecamy-lamine, and alpha-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 alpha,beta-methylene adenosine triphosphate (alpha,beta-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-beta-erythroidine, whereas alpha-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 alpha 4 beta 2, alpha 3 beta 4, and alpha 7 sub-types of nAChRs contribute to the enhancement effect of nicotine on EFS-induced contractile responses.