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  • Petersson, JoelUppsala universitet,Institutionen för medicinsk cellbiologi (författare)

eNOS involved in colitis-induced mucosal blood flow increase

  • Artikel/kapitelEngelska2007

Förlag, utgivningsår, omfång ...

  • American Physiological Society,2007
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:uu-13069
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-13069URI
  • https://doi.org/10.1152/ajpgi.00357.2007DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • 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-omega-nitro-Larginine (L-NNA) or the inducible NOS (iNOS) inhibitor L-N-6-(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.

Ämnesord och genrebeteckningar

  • trinitrobenzene sulfonic acid
  • dextran sulfate sodium
  • inducible nitric oxide synthase
  • neuronal nitric oxide synthase
  • MEDICINE
  • MEDICIN

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Schreiber, OlofUppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)olosc876 (författare)
  • Steege, Andreas (författare)
  • Patzak, Andreas (författare)
  • Hellsten, AnnaUppsala universitet,Institutionen för medicinsk cellbiologi (författare)
  • Phillipson, MiaUppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)mjo07958 (författare)
  • Holm, LenaUppsala universitet,Institutionen för medicinsk cellbiologi(Swepub:uu)pho23887 (författare)
  • Uppsala universitetInstitutionen för medicinsk cellbiologi (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:American Journal of Physiology - Gastrointestinal and Liver Physiology: American Physiological Society293:6, s. G1281-G12870193-18571522-1547

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