Nicotine Potentiates the Electrical Field Stimulation-Evoked Contraction of Non-Pregnant Rabbit Myometrium

Abstract

The women who smoke have lower fertility rates which might be due to harmful effects of nicotine on tubal function and menstrual cycle. Although the uterine contractility of the non-pregnant uterus plays an important role in the human reproduction process, the influence of nicotine on the contractile responses in uterus is not known. Nicotine increases the release of neurotransmitters following nerve stimulation both in the central and peripheral nervous system through acting on nicotinic acetylcholine receptors (nAchRs). The aim of this study was to examine whether the electrical field stimulation (EFS)-evoked contraction is altered in rabbit myometrium strips in the presence of nicotine to evaluate the changes in contractility. EFS-evoked contractile responses were recorded from myometrium strips obtained from non-pregnant rabbits in the absence and presence of nicotine. Nicotine led to the increase in the amplitudes of the EFS-evoked contractile responses in a dose-dependent manner. Therefore, the effects of hexamethonium, cadmium, indomethacin, atropine, and N(omega)-Nitro-L-arginine methyl ester hydrochloride were tested on the EFS-evoked contractions in the absence or presence of nicotine to clarify the mechanisms of nicotine-induced potentiation in EFS-evoked contractile responses. Indomethacin, a non-selective cyclooxygenase inhibitor, and hexamethonium, a ganglionic blocker, inhibited nicotine-induced increase in EFS-evoked responses, whereas other chemicals produced no effect. These results suggest that nicotine-induced potentiation may be mediated by nAchRs and prostaglandins. In conclusion, failure of quiescence in the uterus due to increased contractility by nicotine might be one of the factors contributing to infertility in female smokers.