Biological flow networks: Antagonism between hydrodynamic and metabolic stimuli as driver of topological transitions

A plethora of computational models have been developed in recent decades to account for the morphogenesis complex biological fluid networks, such as capillary beds. Contemporary adaptation are based on optimization schemes where networks react and adapt vessel conductance toward given flow patterns. Recent numeric studies network morphogenesis, incorporating uptake metabolites by embedding tissue, indicated this conventional approach be insufficient. Here, we systematically study a hybrid model intended generate space-filling perfusion well optimal filtration metabolites. As result, find hydrodynamic stimuli (wall-shear stress) (uptake metabolites) antagonistic hydrodynamically optimized systems suboptimal qualities vice versa. We show that switch between regimes is typically accompanied with transition topologically redundant meshes spanning trees. Depending metabolite demand capabilities adapting further demonstrate existence nullity reentrance function dissipation development compromised phenotypes dangling nonperfused vessels bottlenecks.