Structural Autoregulation of Terminal Vascular Beds

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Abstract
-It is widely accepted that the early phase of primary hypertension is characterized by elevated cardiac output, whereas in later stages the increased blood pressure is due to increased peripheral resistance. To study long-term effects of increased blood flow on peripheral resistance, structural adaptation of microvascular networks in response to changes in blood flow was simulated using a previously developed theoretical model. The diameter of each vessel segment was assumed to change in response to local levels of shear stress, transmural pressure, a metabolic stimulus dependent on blood flow rate, and a conducted stimulus. Network morphologies and topologies were derived from intravital microscopy of the rat mesentery. Adaptive responses to the 4 stimuli were quantitatively balanced to yield stable and realistic distributions of vascular diameters and blood flow rates when the total flow rate was set to observed levels. To simulate effects of increased cardiac output, network flow resistance after structural adaptation was determined for a range of flow rates. Resistance increased with increasing flow, and increases in pressure were up to 3-fold greater than proportional to the increases in flow. According to the model, flow-dependent changes of network resistance result mainly from the vascular response to transmural pressure, which also causes arteriovenous asymmetry of diameters and pressure drops. Therefore, in vascular beds that exhibit arteriovenous asymmetry, increased flow may trigger increased flow resistance by a mechanism involving the tendency of vascular segments to reduce their luminal diameters in response to increased transmural pressure.