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

Journal Article (Journal Article)

To study whether a sepsis-induced increase in des-Arg9-bradykinin (des-Arg9-BK) and bradykinin (BK) B1-receptor activity participates in the observed increase in pulmonary vascular resistance in neonatal group B streptococcal sepsis (GBS), isometric force bioassays of pulmonary artery (PA) rings were studied, after 4-h exposure to either Krebs or GBS, by using the following protocols: 1) BK dose-response curve, 2) vascular response to BK with NG-nitro-L-arginine methyl ester (L-NAME), and 3) response to des-Arg9-BK (BK metabolite and B1 agonist). PA rings exposed to BK resulted in contraction in the GBS group and a decrease in resting tension in the Control group (P = 0.034) at a concentration of 10(-5) M. GBS-treated PA rings contracted more to des-Arg9-BK than did Controls (P < 0.001). BK (10(-6) M) relaxed preconstricted PA rings incubated in GBS less than BK relaxed Controls (P < 0.001), and preincubation with L-NAME decreased relaxation in both. These results suggest that GBS decreased endothelium-dependent BK relaxation and increased contractile response to des-Arg9-BK. We speculate that this occurs secondary to upregulation of B1 receptors reflected by B1-agonist-mediated PA contraction.

Full Text

Duke Authors

Cited Authors

  • Whitehurst, RM; Laskey, R; Goldberg, RN; Herbert, D; Van Breemen, C

Published Date

  • January 1999

Published In

Volume / Issue

  • 86 / 1

Start / End Page

  • 61 - 65

PubMed ID

  • 9887113

International Standard Serial Number (ISSN)

  • 8750-7587

Digital Object Identifier (DOI)

  • 10.1152/jappl.1999.86.1.61


  • eng

Conference Location

  • United States