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The kinin B2 receptor, which is constitutively expressed in a large number of tissues, mediates most of the known effects of bradykinin (BK). Normally undetectable in healthy tissues, the B1 receptor is strongly over-expressed under pathological conditions. BK is an important mediator in renal homeostasis and is mainly known for its natriuretic and vasodilatory effects. Recent data evidenced a role for BK in many other biological processes, such as apoptosis, development, extracellular matrix regulation and angiogenesis. In a first step to better understand how BK and its receptors could be involved in such a large variety of biological effects, we used microarray analysis to identify, under physiological conditions, the global renal gene expression profile in mice lacking either the kinin B1 or B2 receptor. Microarray experiments were performed using Agilent Mouse Oligonucleotide Microarrays (21 000 genes/microarray). Interestingly, there was a considerable number of mostly downregulated genes in both BK null mouse models compared with wild-type mice. Furthermore, a number of genes that are known to be implicated in renal physiology and/or pathology were differentially expressed in the BK null mice, which is indicative of the important role of both BK receptors in renal function.

Renal gene expression profiling using kinin B1 and B2 receptor knockout mice reveals comparable modulation of functionally related genes