| Research Abstract |
The primary purpose of microcirculation is to transport nutrients and oxygen and to remove metabolic waste products from the tissue. It is also well-known that the fundamental mechanism for vascular control is the local regulation of the basal vascular tone, which is reinforced by bolld pressure and counteracted by tissue metabolites. Thus, the well-being of the tissue depends on the circulatory transport process, which is governed by many functional parameters of the microcirculation, such as blood folw, blood volume, intravascular and extravascular pressures, and capillary permeabillity. In this respect, it is important to elucidate the mechanism of microcirculatory local regulation in order to understand the pathophysiology of the disorders in oral circulation. Our laboratory has helped to pioneer and develop the hypothesis that kinins play an important role in the control of oral circulation via the salivary gland functions. Mounting evidences from other laboratories have also implicated kinins and their related reactions in local regulation of microcirculation. Now we consider the evidence supporting the hypothesis that kinins and their metabolites (des-Arg^9-bradykinin and des-Arg^<10>-kallidin) may actively participate in the pathophysiological vessel wall response in the oral region; particularly, bradykinin may exert the effect via prostaglandin synthesis through B_2-kinin receptor activation in blood flow of dental pulp. There is also possibility that endotoxin (lipopolysaccharide extracted from E. coli), an initiator of chronic gingivitis, may promote the release of kinins and/or induce the formation of kinin-receptors in vascular system in oral region. Thus, the participation of kinins and their related endogenous vasoactive substances in oral microcirculatory disorders appears to have been clearly established.
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