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,
Departamentos de
*
Bioquímica e Imunologia, e
Fisiologia e Biofísica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, and
Centro Universitário de Belo Horizonte, Belo Horizonte, Minas Gerais, Brazil;
Departmento de Biofísica, Escola Paulista de Medicina, São Paulo, São Paulo, Brazil; and
¶
Molecular Biology of Peptide Hormones Group, Department of Neuroscience, Max-Delbrück-Center for Molecular Medicine, Berlin-Buch, Germany
The administration of bradykinin may attenuate ischemia and reperfusion (I/R) injury by acting on B2Rs. Blockade of B2R has also been shown to ameliorate lesions associated with I/R injury. In an attempt to explain these contradictory results, the objective of the present work was to investigate the role of and interaction between B1 and B2 receptors in a model of intestinal I/R injury in mice. The bradykinin B2R antagonist (HOE 140) inhibited reperfusion-induced inflammatory tissue injury and delayed lethality. After I/R, there was an increase in the expression of B1R mRNA that was prevented by HOE 140. In mice that were deficient in B1Rs (B1R-/- mice), inflammatory tissue injury was abrogated, and lethality was delayed and partially prevented. Pretreatment with HOE 140 reversed the protective anti-inflammatory and antilethality effects provided by the B1R-/- phenotype. Thus, B2Rs are a major driving force for B1R activation and consequent induction of inflammatory injury and lethality. In contrast, activation of B2Rs may prevent exacerbated tissue injury and lethality, an effect unmasked in B1R-/- mice and likely dependent on the vasodilatory actions of B2Rs. Blockade of B1Rs could be a more effective strategy than B2 or B1/B2 receptor blockade for the treatment of the inflammatory injuries that follow I/R.
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