Influence of group B streptococci on piglet pulmonary artery response to bradykinin

To study whether a sepsis-induced increase in des-Arg(9)-bradykinin (des-Ar g(9)-BK) and bradykinin (BK) B-1-receptor activity participates in the obse rved increase in pulmonary vascular resistance in neonatal group B streptoc occal sepsis (GBS), isometric force bioassays of pulmonary artery (PA) ring s were studied, after 4-h exposure to either Krebs or GBS, by using the fol lowing protocols: 1) BK dose-response curve, 2) vascular response to BK wit h N-G-nitro-L-arginine methyl ester (L-NAME), and 3) response to des-Arg(9) -BK (BK metabolite and B, agonist). PA rings exposed to BK resulted in cont raction in the GBS group and a decrease in resting tension in the Control g roup (P = 0.034) at a concentration of 10(-5) M. GBS-treated PA rings contr acted more to des-Arg(9)-BK than did Controls (P < 0.001). BK (10(-6) M) re laxed preconstricted PA rings incubated in GBS less than BK relaxed Control s (P < 0.001), and preincubation with L-NAME decreased relaxation in both. These results suggest that GBS decreased endothelium-dependent BK relaxatio n and increased contractile response to des-Arg(9)-BK. We speculate that th is occurs secondary to upregulation of B-1 receptors reflected by B-1-agoni st-mediated PA contraction.