Bradykinin B(1) receptor-mediated changes in renal hemodynamics during endotoxin-induced inflammation.

Kinins have been shown to influence renal hemodynamics and function. Under physiologic conditions, most kinin effects involve bradykinin B(2) receptors, but bradykinin B(1) receptors are often induced during inflammation. The purpose of this study was to examine in vivo the effects of bradykinin B(1) receptor activation on renal hemodynamics under normal and inflammatory conditions. In anesthetized rats, activation of bradykinin B(1) receptors by arterial infusion of bradykinin B(1) receptor agonist des-Arg(9)-bradykinin reduced renal plasma flow and GFR. Prior administration (18 h) of lipopolysaccharide to induce inflammation resulted in a larger bradykinin B(1) receptor-induced reduction in renal plasma flow. Values of other parameters remained unchanged, thus resulting in an increased filtration fraction. The presence and the functionality of the bradykinin B(1) receptor at the level of glomerular afferent and efferent arterioles were studied by mRNA expression analysis and intracellular calcium ([Ca(2+)](i)) mobilization studies. Stimulation with des-Arg(9)-bradykinin of microdissected afferent arterioles from control and lipopolysaccharide-treated rats induced [Ca(2+)](i) mobilization without any significant difference in amplitude between control and lipopolysaccharidetreated rats. However, des-Arg(9)-bradykinin only induced [Ca(2+)](i) mobilization in efferent arterioles from lipopolysaccharide-treated rats. It is suggested that activation of bradykinin B(1) receptors located along the efferent arteriole may participate in the modification of renal hemodynamics in inflammatory states.