title: Role of inflammatory mediators in colonic smooth muscle function in ulcerative colitis.
abstract: Patients with ulcerative colitis have a decrease in colonic motility which may increase their diarrheal symptoms. Studies in patients with ulcerative colitis showed that the postprandial spike response was slightly decreased and the intraluminal pressure response was absent. In vitro studies showed that the circular smooth muscle, obtained from patients with ulcerative colitis or from a rabbit model of experimental colitis, generated decreased force compared to muscle not associated with mucosal inflammation. The decrease in muscle contraction was observed with bethanechol stimulation or electrical field stimulation. Since the response to an increased extracellular concentration of potassium [( K+]0) was also diminished, the decreased response appears to be caused by an abnormality in the intrinsic contractile mechanism of colonic smooth muscle. Further studies are necessary to determine if metabolic abnormalities are present in the colonic muscle in patients with colitis.
mesh_terms: D000818:Animals; D018723:Bethanechol; D001626:Bethanechol Compounds / Q000494:pharmacology; D003093:Colitis, Ulcerative / Q000209:etiology / Q000503:physiopathology*; D003106:Colon / Q000503:physiopathology*; D004558:Electric Stimulation; D005769:Gastrointestinal Motility; D006801:Humans; D066298:In Vitro Techniques; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000503:physiopathology*; D011817:Rabbits
chemical_list: D001626:Bethanechol Compounds; D018723:Bethanechol