RGD Reference Report - Role of the bradykinin B2 receptor for the local and systemic inflammatory response that follows severe reperfusion injury. - Rat Genome Database

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Role of the bradykinin B2 receptor for the local and systemic inflammatory response that follows severe reperfusion injury.

Authors: Souza, DG  Pinho, V  Pesquero, JL  Lomez, ES  Poole, S  Juliano, L  Correa A, JR  De A Castro, MS  Teixeira, MM 
Citation: Souza DG, etal., Br J Pharmacol. 2003 May;139(1):129-39.
RGD ID: 1641806
Pubmed: PMID:12746231   (View Abstract at PubMed)
PMCID: PMC1573815   (View Article at PubMed Central)
DOI: DOI:10.1038/sj.bjp.0705200   (Journal Full-text)

1. Bradykinin (BK) appears to play an important role in the development and maintenance of inflammation. Here, we assessed the role of the BK B(2) receptor for the injuries that occur after ischemia and reperfusion (I/R) of the territory irrigated by the superior mesenteric artery. 2. Tissue (lung and duodenum) kallikrein activity increased after ischemia with greater enhancement after reperfusion. A selective inhibitor of tissue kallikrein, Phenylacetyl-Phe-Ser-Arg-N-(2,3-dinitrophenyl)-ethylenediamine (TKI, 0.001-10 mg ml(-1)), inhibited kallikrein activity in a concentration-dependent manner in vitro. In vivo, pretreatment with TKI (30 mg kg(-1)) prevented the extravasation of plasma and the recruitment of neutrophils. 3. Similarly, the bradykinin B(2) receptor antagonists, HOE 140 (0.01-1.0 mg kg(-1)) or FR173657 (10.0 mg kg(-1)), inhibited reperfusion-induced increases in vascular permeability and the recruitment of neutrophils in the intestine and lungs. 4. In a model of more severe I/R injury, HOE 140 (1.0 mg kg(-1)) inhibited the increase in vascular permeability, neutrophil recruitment, haemorrhage and tissue pathology. Furthermore, HOE 140 significantly inhibited the elevations of TNF-alpha in tissue and serum and partially prevented lethality. This was associated with an increase in the concentrations of IL-10 in tissue and serum. 5. Thus, our results demonstrate that, following intestinal I/R injury, there is an increase in tissue kallikrein activity and activation of BK B(2) receptors. B(2) receptor activation is essential for the development of inflammatory tissue injury and lethality. These results contrast with those of others showing that BK mostly exerts a protective role during I/R injury.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
KLK1HumanReperfusion Injury  ISOKlk1 (Rattus norvegicus) RGD 
Klk1RatReperfusion Injury  IEP  RGD 
Klk1MouseReperfusion Injury  ISOKlk1 (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Klk1  (kallikrein 1)

Genes (Mus musculus)
Klk1  (kallikrein 1)

Genes (Homo sapiens)
KLK1  (kallikrein 1)

Objects referenced in this article
Gene Klk1c12 kallikrein 1-related peptidase C12 Rattus norvegicus

Additional Information