HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/6/G1281    most recent 00357.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Petersson, J. Articles by Holm, L. Search for Related Content PubMed PubMed Citation Articles by Petersson, J. Articles by Holm, L.

INFLAMMATION/IMMUNITY/MEDIATORS

eNOS involved in colitis-induced mucosal blood flow increase

¹Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden; and ²Institute of Vegetative Physiology, Charité-Universitätsmedizin Berlin, Berlin, Germany

Submitted 8 August 2007 ; accepted in final form 17 October 2007

The role of NO in inflammatory bowel disease is controversial. Studies indicate that endothelial nitric oxide synthase (eNOS) might be involved in protecting the mucosa against colonic inflammation. The aim of this study was to investigate the involvement of nitric oxide (NO) in regulating colonic mucosal blood flow in two different colitis models in rats. In anesthetized control and colitic rats, the distal colon was exteriorized and the mucosa visualized. Blood flow (laser-Doppler flowmetry) and arterial blood pressure were continuously monitored throughout the experiments, and vascular resistance was calculated. Trinitrobenzene sulfonic acid (TNBS) or dextran sulfate sodium (DSS) was used to induce colitis. All groups were given the NOS inhibitor N-nitro-L-arginine (L-NNA) or the inducible NOS (iNOS) inhibitor L-N⁶-(1-iminoethyl)-lysine (L-NIL). iNOS, eNOS, and neuronal NOS (nNOS) mRNA in colonic samples were investigated with real-time RT-PCR. Before NOS inhibition, colonic mucosal blood flow, expressed as perfusion units, was higher in both colitis models compared with the controls. The blood flow was reduced in the TNBS- and DSS-treated rats during L-NNA administration but was not altered in the control group. Vascular resistance increased more in the TNBS- and DSS-treated rats than in the control rats, indicating a higher level of vasodilating NO in the colitis models. L-NIL did not alter blood pressure or blood flow in any of the groups. iNOS and eNOS mRNA increased in both colitis models, whereas nNOS remained at the control level. TNBS- and DSS-induced colitis results in increased colonic mucosal blood flow, most probably due to increased eNOS activity.

Trinitrobenzene sulfonic acid; dextran sulfate sodium; inducible nitric oxide synthase; neuronal nitric oxide synthase

This article has been cited by other articles:

				W.-H. Kan, J.-T. Hsu, M. G. Schwacha, M. A. Choudhry, R. Raju, K. I. Bland, and I. H. Chaudry Selective inhibition of iNOS attenuates trauma-hemorrhage/resuscitation-induced hepatic injury J Appl Physiol, October 1, 2008; 105(4): 1076 - 1082. [Abstract] [Full Text] [PDF]