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

Author:

Cervenka Ludek1,Harrison-Bernard Lisa M.1,Dipp Susana1,Primrose Ginny1,Imig John D.1,El-Dahr Samir S.1

Affiliation:

1. From the Departments of Pediatrics (S.D., S.S.E.-D.) and Physiology (L.C., L.M.H.-B., G.P., J.D.I.), Tulane University School of Medicine, New Orleans, La.

Abstract

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 <0.05) at 2, 3, and 4 months versus other groups. MAP was also higher in HS/B 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 <0.05). Kidney renin and angiotensin type 1 receptor mRNA levels were not different. Additional studies showed that a delay in the initiation of HS until after birth was accompanied by later development of hypertension, although postnatal discontinuation of HS resulted in a gradual return of BP to normal values by 4 months of age. The results demonstrate that (1) kinins protect the developing animal from salt-sensitive hypertension, (2) lack of B 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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Internal Medicine

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