Kitazawa T, Kikui S, Taneike T, Ohaga A
Department of Veterinary Pharmacology, Faculty of Dairy Science, Rakuno Gakuen University, Ebe Tsu, Japan.
Gen Pharmacol. 1996 Jun;27(4):655-64. doi: 10.1016/0306-3623(95)02039-x.
To clarify the physiological role of motilin in the pig gastrointestinal (GI) tract, effect of Leu13-porcine motilin (LMT) on the contractility of GI smooth muscle was investigated in studies using isolated muscle strips and dispersed muscle cells. LMT produced no contraction in either longitudinal muscle (LM) or circular muscle (CM) of the stomach (fundus, corpus, antrum), duodenum, ileum and colon even at 1 microM. Pretreatment with LMT (1 nM-1 microM) did not potentiate the contractile response to acetylcholine (ACh) in each muscle strip. Dispersed cells from the duodenum responded to ACh in a concentration-dependent manner (EC50 = 10 pM), but not to LMT even at a high concentration (10 microM). Electrical field stimulation (EFS) caused a frequency-dependent (0.2-10 Hz) contraction of the duodenal LM that was almost completely inhibited by atropine or tetrodotoxin. EFS caused the relaxation of duodenal CM in a frequency-dependent manner (0.1-10 Hz). This relaxation was not inhibited by atropine, propranolol, phentolamine or guanethidine, indicating the involvement of noncholinergic, nonadrenergic (NCNA) nerves. NG-nitro L-arginine methylester (L-NAME, 100 microM) attenuated the EFS-induced relaxation and the inhibition at low frequency was larger than that at high frequency. L-Arginine prevented the inhibition by L-NAME but D-arginine did not. LMT (1 nM-1 microM) had no influence on EFS-induced cholinergic contraction of LM and EFS-induced NCNA relaxation of CM layer. The present in vitro studies indicate that motilin is ineffective in producing contraction and in modulating the autonomic neuroeffector transmission of the pig GI smooth muscle, and suggest that pig GI smooth muscle lacks functional motilin receptors.
为阐明胃动素在猪胃肠道中的生理作用，在使用离体肌条和分散肌细胞的研究中，考察了亮氨酸-13-猪胃动素（LMT）对胃肠道平滑肌收缩性的影响。即使在1微摩尔浓度下，LMT对胃（胃底、胃体、胃窦）、十二指肠、回肠和结肠的纵行肌（LM）或环行肌（CM）均未产生收缩作用。用LMT（1纳摩尔 - 1微摩尔）预处理并未增强各肌条对乙酰胆碱（ACh）的收缩反应。十二指肠的分散细胞对ACh呈浓度依赖性反应（半数有效浓度 = 10皮摩尔），但即使在高浓度（10微摩尔）下对LMT也无反应。电场刺激（EFS）引起十二指肠纵行肌频率依赖性（0.2 - 10赫兹）收缩，该收缩几乎完全被阿托品或河豚毒素抑制。EFS引起十二指肠环行肌频率依赖性（0.1 - 10赫兹）舒张。这种舒张不受阿托品、普萘洛尔、酚妥拉明或胍乙啶抑制，表明涉及非胆碱能、非肾上腺素能（NCNA）神经。N-硝基-L-精氨酸甲酯（L-NAME，100微摩尔）减弱了EFS诱导的舒张，低频时的抑制作用大于高频时。L-精氨酸可防止L-NAME的抑制作用，但D-精氨酸则不能。LMT（1纳摩尔 - 1微摩尔）对EFS诱导的纵行肌胆碱能收缩和EFS诱导的环行肌层NCNA舒张均无影响。目前的体外研究表明，胃动素在引起猪胃肠道平滑肌收缩及调节自主神经效应器传递方面无效，并提示猪胃肠道平滑肌缺乏功能性胃动素受体。
