Terminal vascular beds continually adapt to hemodynamic and metabolic (e.g. PO2) conditions to fulfill their primary task of adequately supplying tissue cells with substrates. Low PO2 has been shown to evoke release of vasoactive substances not only by the tissue itself (e.g. adenosine) but also by erythrocytes (e.g. ATP). Here, we investigate the relative impact of metabolic signals originating from the vessels and the tissue. A theoretical model of structural angioadaptation based on experimental data of microvascular networks (>500 segments) of the rat mesentery was used. In the model, any vessel is assumed to change its diameter and wall thickness in response to wall shear stress, transmural pressure and a metabolic stimulus. This metabolic stimulus was represented by (A) tissue PO2 or (B) vascular PO2. Quality of these assumptions was determined by estimating average and systematic deviations between predicted and measured vessel diameters and blood flow velocities. (B) led to both lower average and systematic (e.g. diameter of supplying arterioles in regions with low vessel density) deviations compared to (A).

In conclusion, the preservation of metabolically adequate microvascular network structures seems to be largely guaranteed by adaptive signals derived from vascular metabolic conditions.