Early Onset Salt-Sensitive Hypertension in Bradykinin B 2 Receptor Null Mice

Open Access
Publisher Website
Google Scholar
Abstract
—Kinins have been implicated in the hemodynamic adaptation to postnatal life. The present study examined the impact of bradykinin B 2 receptor (B 2 R) gene disruption on the postnatal changes in blood pressure (BP) and the susceptibility to early onset salt-sensitive hypertension in mice. B 2 R null (−/−) and wild-type (+/+) mice were fed normal (NS, 1% NaCl) or high (HS, 5% NaCl) salt diets during pregnancy. After birth, the pups remained with their mothers until they were weaned and were subsequently continued on the respective maternal salt intake until 4 months of age. The age-related changes at 3 and 4 months in tail-cuff BP and anesthetized mean arterial pressure at 4 months were not different in NS/B 2 R −/− and NS/B 2 R +/+ mice. However, there was a mild increase in BP in NS/B 2 R −/− at 2 months versus NS/B 2 R +/+ . In contrast, HS/B 2 R −/− mice manifested early onset and persistent elevations of tail-cuff BP ( P 2 R −/− than HS/B 2 R +/+ , NS/B 2 R −/− , and NS/B 2 R +/+ (91±3 versus 75±5, 74±2, and 70±2 mm Hg, respectively; P 2 R from early development does not alter the maturation of BP under conditions of normal sodium intake, and (3) exposure to a HS diet during fetal life is not sufficient in itself to induce long-term hypertension in either wild-type or B 2 R null mice.