Vol. 86, Issue 1, 61-65, January 1999
Influence of group B streptococci on piglet pulmonary artery
response to bradykinin
Richard M.
Whitehurst1,
Rachel
Laskey2,
Ronald N.
Goldberg1,
Donald
Herbert3, and
Cornelius
Van
Breemen4
1 Division of Neonatology,
Department of Pediatrics, University of Miami School of Medicine,
Miami, Florida 33101; 2 The Upjohn
Company, Kalamazoo, Michigan 49006;
3 Department of Radiology,
University of South Alabama, Mobile, Alabama 36688; and
4 Department of Pharmacology
and Therapeutics, University of British Columbia, Vancouver, British
Columbia, Canada V6T 1Z3
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
(106 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.
newborn; persistent pulmonary hypertension of the newborn; bradykinin B1-receptor; des-Arg9 bradykinin; sepsis
