title: Evidence against a systemic arterial defect in patients with inflammatory bowel disease.
abstract: BACKGROUND
  Despite increasing interest in local microvascular alterations associated with inflammatory bowel disease (IBD), the potential contribution of a primary systemic vascular defect in the etiology of IBD is unknown. We compared reactivity of large diameter mesenteric arteries from segments affected by Crohn disease (CD) or ulcerative colitis (UC) to an uninvolved vascular bed in both IBD and control patients.
  
  
  METHODS
  Mesenteric and omental arteries were obtained from UC, CD, and non-IBD patients. Isometric arterial contractions were recorded in response to extracellular potassium (K(+)) and cumulative additions of norepinephrine (NE). In addition, relaxation in response to pinacidil, an activator of adenosine triphosphate-sensitive K(+) channels was examined.
  
  
  RESULTS
  Contraction to K(+) and sensitivity to NE were not significantly different in arteries from CD, UC, and controls. Relaxation to pinacidil was also similar between groups.
  
  
  CONCLUSIONS
  Potassium-induced contractions and sensitivity to NE and pinacidil were not significantly different in large diameter mesenteric and omental arteries obtained from IBD patients. Furthermore, there was no significant difference in the sensitivity to K(+), NE, and pinacidil between mesenteric and omental arteries of CD and UC patients and those from non-IBD patients. Our results suggest an underlying vascular defect systemic to CD or UC patients is unlikely to contribute to the etiology of IBD.
authors.affiliation: Department of Surgery, University of Vermont College of Medicine, Burlington, Vermont.
authors.forename: Luke A
authors.initials: LA
authors.lastname: Neill
authors.affiliation: Department of Pharmacology, College of Medicine, University of Vermont, Burlington, Vermont.
authors.forename: Christine M
authors.initials: CM
authors.lastname: Saundry
authors.affiliation: Department of Surgery, College of Medicine, University of Vermont, Burlington, Vermont. Electronic address: neil.hyman@vtmednet.org.
authors.forename: Neil H
authors.initials: NH
authors.lastname: Hyman
authors.affiliation: Department of Pharmacology, College of Medicine, University of Vermont, Burlington, Vermont; Department of Surgery, College of Medicine, University of Vermont, Burlington, Vermont.
authors.forename: George C
authors.initials: GC
authors.lastname: Wellman
mesh_terms: D015220:Calcium Channels / Q000502:physiology; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000209:etiology / Q000503:physiopathology*; D008638:Mesenteric Arteries / Q000503:physiopathology*; D009638:Norepinephrine / Q000494:pharmacology; D020110:Pinacidil / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D015220:Calcium Channels; D020110:Pinacidil; D011188:Potassium; D009638:Norepinephrine
keywords: Crohn disease; Inflammatory bowel disease; Mesenteric artery; Norepinephrine; Pinacidil; Potassium; Ulcerative colitis