Mechanisms Mediating the Vasoactive Effects of the B1 Receptors of Bradykinin

ABSTRACT—Bradykinin normally exerts its vasodilatory effect via the B2 receptor (B2R), but in this receptor’s absence, the B1 receptor becomes expressed and activated. To explore the mechanism of B1R-mediated vasodilation, 8 groups of B2R gene–knockout mice received a 2-week infusion of a B1R antagonist (300 μg · kg · d) or vehicle (groups 1 and 2), B1R antagonist or vehicle plus NO inhibition with Nω-nitro-l-arginine methyl ester (groups 3 and 4), B1R antagonist or vehicle plus cyclooxygenase inhibition with indomethacin (groups 5 and 6), or B1R antagonist or vehicle plus blockade of vasoconstricting prostaglandin (PG) H2 and thromboxane A2 (TxA2) with SQ29548 (groups 7 and 8). The B1R antagonist produced significant (P