© 2001 American Heart Association, Inc.
Integrative Physiology |
Decreased Flow-Dependent Dilation in Carotid Arteries of Tissue Kallikrein–Knockout Mice
From the Institut National de la Santé et de la Recherche Médicale, Unit 541 (S.B., E.M., B.I.L., C.M.B.), Hôpital Lariboisière, and Unit 367 (P.M., M.B.-F., F.A.-G.), Paris, France.
Correspondence to Chantal M. Boulanger, PhD, INSERM Unit 541, Hôpital Lariboisière, 41 Bd de la Chapelle, F-75475 Paris Cedex 10, France. E-mail chantal.boulanger{at}inserm.lrb.ap-hop-paris.fr
Abstract— Flow-dependent
dilation is a fundamental mechanism by which large arteries ensure
appropriate blood supply to tissues. We investigated whether or not the
vascular kallikrein-kinin system, especially tissue kallikrein (TK),
contributes to flow-dependent dilation by comparing wild-type and
TK-knockout mice in which the presence or absence of TK expression was
verified. We examined in vitro changes in the outer diameter of
perfused carotid arteries from TK+/+ and
TK-/- mice. In both groups, exogenous
bradykinin caused a similar dilation that was abolished by the
B2 receptor antagonist HOE-140, as
well as by the NO synthase inhibitor
N
-nitro-L-arginine
methyl ester. However, purified kininogen dilated only
TK+/+ arteries, demonstrating the essential
role of TK in the vascular formation of kinins. In
TK+/+ arteries, increasing intraluminal flow
caused a larger endothelium-dependent dilation than
that seen in TK-/-. In both strains the
flow response was mediated by NO and by
endothelium-derived hyperpolarizing factor, whereas in
TK-/- vasoconstrictor prostanoids
participated as well. HOE-140 impaired flow-dependent dilation in
TK+/+ arteries while showing no effect in
TK-/-. This compound reduced the flow
response in TK+/+ arteries to a level
similar to that in TK-/-. After NO
synthase inhibition, HOE-140 no longer affected the response of
TK+/+. Impaired flow-dependent dilation was
also observed in arteries from knockout mice lacking bradykinin
B2 receptors as compared with wild-type animals.
This study demonstrates the active contribution of the vascular
kallikrein-kinin system to one-third of the flow-dependent dilation
response via activation of B2 receptors coupled
to endothelial NO release.
Key Words: bradykinin • kininogen • flow-dependent vasodilation • endothelium • bradykinin B2 receptor
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