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Am J Physiol Heart Circ Physiol (January 30, 2003). doi:10.1152/ajpheart.01150.2002
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Submitted on January 8, 2003
Accepted on January 24, 2003

Decreased Renal NO Excretion and Reduced Glomerular Tuft Area in Mice Lacking the Bradykinin B2 Receptor

Joost P Schanstra1, Johan Duchene1, Francoise Praddaude1, Patrick Bruneval2, Ivan Tack1, Jacques Chevallier2, Jean-Pierre Girolami1, and Jean-Loup Bascands1*

1 Inserm U388, Institut Louis Bugnard, Toulouse, France
2 Inserm U430, Hopital Broussais, Paris, France

* To whom correspondence should be addressed. E-mail: bascalou{at}toulouse.inserm.fr.

Bradykinin B2 receptor knockout mice (B2-/-) have been useful to study the role of bradykinin under pathological conditions. Using these mice it was shown that bradykinin plays an important role in angiogenesis, heart failure, salt induced hypertension and kidney fibrosis. Data on the role of the bradykinin B2 receptor under physiological conditions using these mice are controversial and scarce since these mice have no typical phenotype. For this reason we have studied, under physiological conditions, renal hemodynamics as well as a number of morphometric glomerular parameters of B2-/- mice on a homogenized genetic background and on mice bred in a pathogen free environment. Backcrossed B2-/- mice had normal blood pressure and normal apparent renal hemodynamics and morphology. However, reduced renal nitrite excretion and glomerular cyclicGMP content were found which was associated to a reduced glomerular capillary surface area. These differences had, however, no detectable effects on renal hemodynamics. These differences between B2-/- and wild type mice might become of importance under pathological conditions as shown by a number of studies using these bradykinin B2 receptor knockout mice.




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