Abstract
Blood vessels are capable of dynamic structural adaptation in which their diameters and wall thicknesses change in response to chronic changes in hemodynamic conditions. Such structural changes can have large effects on vascular resistance to blood flow. Structural responses to hemodynamic stresses, i.e., wall shear stress resulting from blood flow and circumferential wall tension resulting from transmural pressure, have been extensively documented. Generally, increased shear stress causes increases in vessel diameter, whereas increased transmural pressure causes opposite effects. Theoretical models have been developed to analyze the consequences of these responses for the behavior of microvascular networks when subjected to changes in systemic circulatory conditions. An initial increase of cardiac output is assumed to increase flow and driving pressure in parallel. According to the models, structural adaptation results in substantially increased overall network flow resistance as flow is increased, and thus amplification of the initially imposed increase in driving pressure. This behavior, resulting from adaptation of individual vessel segments to intravascular pressure, is consistent with data on the development of hypertension, which suggest that an increase in cardiac output precedes the increase in peripheral resistance that is characteristic of established hypertension. Thus, vascular sensitivity to circumferential wall stress may play a crucial role in the development of hypertension. Microcirculation(2002) 9,305–314. doi: 10.1038/sj.mn.7800144