Role of the Bradykinin B2 Receptor in Salt-Induced Hypertension
The kallikrein-kinin system may contribute to blood pressure (BP) regulation via its vasodilatory, natriuretic and diuretic activity. In order to explore the role of bradykinin in this respect, we studied knockout mice (n=16) with deleted gene for the B2 receptor of bradykinin (BKB2R -/-), submitted to subtotal nephrectomy (SN) and dietary salt-loading, in comparison to their wildtype counterparts (BKB2R +/+, n=10). Systolic BP mmHg (by tail cuff), heart rate (HR b/min), plasma catecholamines, (NEPI, EPI ng/ml) and heart weight/body weight ratio (mg/g) are shown in the Table below. *p<0.05 knockouts vs wildtype. Thus, the BKB2Rgene knockout mice had higher BP at baseline and developed more severe hypertension. Moreover, they became hypertensive in 19±2 days versus 28±2 days for the wildtype (p<0.05). We conclude that bradykinin, acting via its B2 receptor, contributes to maintenance of normotension and protects against salt-induced hypertension.