Kitazawa T, Onodera C, Taneike T
Department of Pharmacology, School of Veterinary Medicine, Rakuno Gakuen University, Ebetsu, Hokkaido 069-8501, Japan.
Neurogastroenterol Motil. 2002 Feb;14(1):3-13. doi: 10.1046/j.1365-2982.2002.00298.x.
The present experiments were designed to determine whether or not endogenous nitric oxide (NO) modifies the contractile response to chicken motilin (ch-MT) in the gastrointestinal (GI) tract (proventriculus and small intestine) of the chicken. ch-MT (1 nmol L(-1)-1 micromol L(-1)) caused contractions of longitudinal muscle strips of the proventriculus through both myogenic and neurogenic (mostly cholinergic) mechanisms. On the other hand, ch-MT (0.1 nmol L(-1)-100 nmol L(-1)) contracted the small intestine (duodenum, jejunum and ileum) only through a myogenic mechanism. L-Nitroarginine methylester (L-NAME) potentiated, and L-arginine inhibited, the ch-MT- induced contraction without affecting the responsiveness of acetylcholine (ACh) or 5-hydroxytryptamine in the proventriculus. Electrical field stimulation (EFS)- and 1,1-dimethyl-4-phenylpiperazinium (DMPP)- induced contractions were also potentiated by L-NAME. The potentiation by L-NAME was prevented by L-arginine but not by D-arginine. However, in the presence of atropine or tetrodotoxin, neither L-NAME nor L-arginine modified the responses to ch-MT and DMPP. In contrast to the proventriculus, L-NAME and L-arginine were both ineffective in modifying the ch-MT-induced contraction in the small intestine. These results indicate that NO synthase inhibition potentiates the contractile response of ch-MT, EFS and DMPP in the chicken proventriculus through reduction of endogenous NO-mediated presynaptic inhibition on neural ACh release. However, NOS inhibition did not modify the myogenic (direct) action of ch-MT in gastric and intestinal smooth muscles of the chicken.
本实验旨在确定内源性一氧化氮（NO）是否会改变鸡胃肠道（前胃和小肠）对鸡胃动素（ch-MT）的收缩反应。ch-MT（1 nmol L⁻¹ - 1 μmol L⁻¹）通过肌源性和神经源性（主要是胆碱能）机制引起前胃纵行肌条收缩。另一方面，ch-MT（0.1 nmol L⁻¹ - 100 nmol L⁻¹）仅通过肌源性机制使小肠（十二指肠、空肠和回肠）收缩。L-硝基精氨酸甲酯（L-NAME）增强，而L-精氨酸抑制ch-MT诱导的收缩，且不影响前胃中乙酰胆碱（ACh）或5-羟色胺的反应性。电场刺激（EFS）和1,1-二甲基-4-苯基哌嗪鎓（DMPP）诱导的收缩也被L-NAME增强。L-NAME的增强作用被L-精氨酸阻止，但不被D-精氨酸阻止。然而，在存在阿托品或河豚毒素的情况下，L-NAME和L-精氨酸均未改变对ch-MT和DMPP的反应。与前胃相反，L-NAME和L-精氨酸在改变ch-MT诱导的小肠收缩方面均无效。这些结果表明，一氧化氮合酶抑制通过减少内源性NO介导的对神经ACh释放的突触前抑制，增强了ch-MT、EFS和DMPP在鸡前胃中的收缩反应。然而，一氧化氮合酶抑制并未改变ch-MT在鸡胃和肠道平滑肌中的肌源性（直接）作用。
