Effects of nicotine on cholinergic transmission in isolated rabbit gastric fundus: to research effects of pyrogallol and antioxidants.

Nicotine having an effect upon presynaptic receptors while having increased the release of Acetylcholine from nerve endings. Our data shows that electrical field stimulation (EFS) dependent Nicotine induced transiently increased contraction of the smooth muscle in the rabbit isolated fundus and Hexamethonium, an antagonist of the neuronal nicotinic receptor, significantly inhibited the contractile response to nicotine on EFS. Furthermore, EFS induced contractions were abolished by Atropine and enhanced by Neostigmine. This data demonstrates that response to Nicotine on EFS proceeds as a result of cholinergic transmission. It is also known that nicotine possesses the property of increasing the formation of reactive oxygen species (ROS). Thus, we decided to investigate whether there is interrelation between the effects of ROS and EFS dependent nicotine induced acetylcholine release. Longitudinal strips of smooth muscle were subjected to electrical field stimulation (EFS) in vitro using stimulus parameters (60 V, 8-32 Hz, 1 ms). The effect of nicotine on EFS responses was then measured in the absence and presence of a Pirogallol, Allopurinol, Deferoxamine and Mannitol. In conlusion, TTX abolished EFS induced contractions. Pirogallol induced decreased EFS-induced contractile response, while there was nosignificant contractile response to nicotine on EFS. At that, Mannitol significantly reduced contractile response to nicotine on EFS only in high concentration. Whereas in small concentrations Mannitol statistically did not cause any results. Deferoxamine and Allopurinol also had no significant response. Key words: acetylcholine, neuronal nicotinic receptors, antioxidants, oxidants.