The blood flow to the peripheral circulation is designed to coordinate the delivery of nutrients with the demands of the tissue. Any increase in blood flow that need occur is the result of an increase in arteriolar diameter. This arteriolar dilation may be die to the effect of one or more vasoactive metabolites released from the tissue. The mechanism by which the arterioles receive the vasodilatory signal from the tissue is not know. The studies described in this proposal are designed to determine whether there is communication between venules and arterioles in such a manner as to regulate arteriolar diameter. Specific hypotheses involve the following questions and measurements: 1) Can there be a diffusion of vasoactive metabolites form a venule to an arteriole in sufficient concentration to affect arteriolar diameter? This will be tested by determining the qualitative and quantitative arteriolar diameter responses during perfusion of an adjacent venule with various vasoactive metabolites. Additional studies will examine whether the diffusion of substances from the venule to the arteriole occurs during changes in the physiological conditions of the tissue. 2) If there is sufficient diffusion of a metabolite from the venule to a crossing arteriole, is the resultant arteriolar dilation localized or is the dilation propagated upstream resulting in larger increases in blood flow? This dilation may be due to a velocity-induced mechanism. 3) Is there a velocity-dependent release of an endothelial derived factor from venules that will affect the diameter of a nearby arteriole? This information will determined by demonstrating the existence of a venular velocity-induced arteriolar vasodilation and then blocking the vasodilation through the use of available EDRF blockers. An important aspect of each of these studies will be to determine the physiological role of each of these mechanisms in regulating arteriolar diameter.
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