Functional sympatholysis and sympathetic escape in a theoretical model for blood flow regulation.

A mathematical simulation of flow regulation in vascular networks is used to investigate the interaction between arteriolar vasoconstriction due to sympathetic nerve activity (SNA) and vasodilation due to increased oxygen demand. A network with 13 vessel segments in series is used, each segment representing a different size range of arterioles or venules. The network includes five actively regulating arteriolar segments with time-dependent diameters influenced by shear stress, wall tension, metabolic regulation, and SNA. Metabolic signals are assumed to be propagated upstream along vessel walls via a conducted response. The model exhibits functional sympatholysis, in which sympathetic vasoconstriction is partially abrogated by increases in metabolic demand, and sympathetic escape, in which SNA elicits an initial vasoconstriction followed by vasodilation. In accordance with experimental observations, these phenomena are more prominent in small arterioles than in larger arterioles when SNA is assumed to act equally on arterioles of all sizes. The results imply that a mechanism based on the competing effects on arteriolar tone of SNA and conducted metabolic signals can account for several observed characteristics of functional sympatholysis, including the different responses of large and small arterioles.