Local control of blood flow is achieved by contraction and dilation of smooth muscle cells in microvessel walls, particularly in arterioles, allowing rapid local responses to changing conditions. Several types of vessel response are involved. In the myogenic response, increased wall tension causes contraction. In the shear-dependent response, increased wall shear stress causes dilation. In the metabolic response, arteriolar diameters change according to the metabolic status sensed at downstream locations (capillaries and venules) after oxygen has been extracted from the blood. Information is transferred upstream along vessel walls by conducted responses, which involve electrical coupling of the cells.
We have developed theoretical models for flow regulation based on a mechanism for the metabolic response in which decreased oxygen levels in venules cause increased release of ATP, which acts on vessel walls to initiate upstream conducted responses leading to vasodilation. This model is used to explore the roles of the various vessel responses in autoregulation, in which flow is almost constant independent of changes in blood pressure, and in metabolic regulation, in which flow is modulated in response to changing metabolic demands. It is shown that autoregulation is achieved by the combined action of myogenic and metabolic responses, which overcome the opposing effect of shear-dependent responses. Metabolic responses are primarily responsible for metabolic flow regulation, but are opposed by the effects of shear-dependent and myogenic responses. The model is based on an explicit description of vascular network structure, and has potential application to the simulation of coronary flow regulation.
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