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— 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 inhibitorN ω -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.

Decreased Flow-Dependent Dilation in Carotid Arteries of Tissue Kallikrein–Knockout Mice