Neurotensin-induced colonic motor responses in dogs: a mediation by prostaglandins.
The effects of systemic infusion of neurotensin (NT) were studied in four dogs fitted with strain-gauge transducers implanted on the ascending and descending colon. The motility index of the colon was enhanced for the duration of the 20 min NT infusion (20 pmol X kg-1 X min-1). Such stimulation was comparable to the colonic motor response elicited by feeding, i.e. the gastrocolic reflex. A period of hypomotility, lasting 40-90 min, occurred after either feeding or completion of NT infusion. Pretreatment with prostaglandin synthetase inhibitors, ketoprofene (KTP) and acetylsalicylic acid (ASA), reduced the magnitude of both the NT- and meal-induced hypermotility responses. The results suggest that the ability of NT to increase colonic motility may involve prostaglandin synthesis and that endogenous prostaglandin may exert a physiologic effect on colonic motor response to feeding. Moreover, these findings support a possible role for NT as one of the mediators involved in the non-neural mediation of the gastrocolic reflex.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D003106:Colon / Q000187:drug effects; D004285:Dogs; D005260:Female; D005502:Food; D005769:Gastrointestinal Motility / Q000187:drug effects*; D007660:Ketoprofen / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects*; D009496:Neurotensin / Q000494:pharmacology*; D011453:Prostaglandins / Q000502:physiology*; D012018:Reflex / Q000187:drug effects
D011453:Prostaglandins; D009496:Neurotensin; D007660:Ketoprofen; D001241:Aspirin