title: Potentiation of motilin-induced contraction by nitric oxide synthase inhibition in the isolated chicken gastrointestinal tract.
abstract: 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.
authors.affiliation: Department of Pharmacology, School of Veterinary Medicine, Rakuno Gakuen University, Ebetsu, Hokkaido 069-8501, Japan. tko-kita@rakuno.ac.jp
authors.forename: T
authors.initials: T
authors.lastname: Kitazawa
authors.forename: C
authors.initials: C
authors.lastname: Onodera
authors.forename: T
authors.initials: T
authors.lastname: Taneike
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D002645:Chickens / Q000502:physiology*; D004064:Digestive System / Q000187:drug effects / Q000201:enzymology*; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005769:Gastrointestinal Motility / Q000187:drug effects / Q000502:physiology; D006145:Guanethidine / Q000494:pharmacology; D066298:In Vitro Techniques; D007421:Intestine, Small / Q000187:drug effects / Q000502:physiology; D008297:Male; D009037:Motilin / Q000494:pharmacology / Q000502:physiology*; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009130:Muscle, Smooth / Q000187:drug effects / Q000201:enzymology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors* / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology; D011531:Proventriculus / Q000187:drug effects / Q000502:physiology
chemical_list: D004791:Enzyme Inhibitors; D009599:Nitroprusside; D009569:Nitric Oxide; D009037:Motilin; D001285:Atropine; D001120:Arginine; D019001:Nitric Oxide Synthase; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester; D006145:Guanethidine