The pluripotent action of kinins has recently become a major topic in the control of oral circulation. In fact, the action of kinins is not consistent in studies performed on isolated blood vessels and whole animals. Depending on the species and anatomical origin of the blood vessels, application of bradykinin (BK) may elicit relaxation, contraction, or no respose at all. This review takes up the following subjects for discussion : vascular response, relation of endothelial cells as mediators, the high potential receptor and the role of a
de novo B
1-receptor formation to kinins. The nature and role of kinins in the regulation of oral vascular tone and hemodynamics have gradually become clear.
1) Kinins may play an important role in regulating the system of microcirculatory hemodynamics in oral tissue and in the genesis of circulatory auto-regulation and reactive hyperemia, and prostaglandins (PGs) -synthesis may be partly concerned in the BK action.
2) Kinins exert their biological actions by activating two receptor systems (the B
1-and B
2-receptors) .
3) The vasodilatory response to kinins is an indirect effect mediated by releases of PGs, leukotrienes, and the endothelium derived relaxing factor (EDRF) from endothelium. Further, kinins produce endothelium-dependent or -independent vasoconstriction.
4) The B
1-receptor seems to be silent
in vivo, but it can be activated
in vivo by noxious stimuli (
e.g. LPS) . The activation appears to be the result of
de novo formation of a B
1-receptor.
Kinins and their metabolites (des-Arg
9-BK and des-Arg
10-kallidin) may participate in the initiation of physiological and pathological vessel wall response.
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