| First Author | Schanstra JP | Year | 2003 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 284 |
| Issue | 6 | Pages | H1904-8 |
| PubMed ID | 12560214 | Mgi Jnum | J:83895 |
| Mgi Id | MGI:2664046 | Doi | 10.1152/ajpheart.01150.2002 |
| Citation | Schanstra JP, et al. (2003) Decreased renal NO excretion and reduced glomerular tuft area in mice lacking the bradykinin B2 receptor. Am J Physiol Heart Circ Physiol 284(6):H1904-8 |
| abstractText | Bradykinin B(2) receptor knockout mice (B(2)-/-) have been useful to study the role of bradykinin under pathological conditions. With the use of 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 B(2) receptor under physiological conditions using these mice are controversial and scarce, because 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 B(2)-/- mice on a homogenized genetic background and on mice bred in a pathogen-free environment. Backcrossed B(2)-/- mice had normal blood pressure and normal apparent renal hemodynamics and morphology. However, reduced renal nitrite excretion and glomerular cGMP content were found, which was associated with a reduced glomerular capillary surface area. These differences had, however, no detectable effects on renal hemodynamics. These differences between B(2)-/- and wild-type mice might become important under pathological conditions as shown by a number of studies using these bradykinin B(2) receptor knockout mice. |
