In resistance-sized arteries, a chronic increase in blood flow leads to increases in arterial structural luminal diameter and arterial wall mass. In this review, we summarize recent evidence that outward remodeling of resistance arteries 1) can help maintain and restore tissue perfusion, 2) is not intimately related to flow-induced vasodilatation, 3) involves transient dedifferentiation and turnover of arterial smooth muscle cells, and 4) is preceded by increased expression of matricellular proteins, which have been shown to promote disassembly of focal adhesion sites. Studies of experimental and physiological resistance artery remodeling involving differential gene expression analyses and the use of knockout and transgenic mouse models can help unravel the mechanisms of outward remodeling.

in arteries, transmural pressure and blood flow influence wall thickness and structural luminal diameter (13, 16, 28, 29, 49). Mathematical modeling, cell and molecular biological approaches, and experiments in genetically modified animals are beginning to shed light on the mechanisms that underlie these arterial remodeling responses. Here, we summarize recent observations concerning flow-induced outward remodeling of resistance arteries. Exploration of this type of arterial structural response might lead to pharmacological treatments to 1) improve collateral perfusion and 2) reverse the inward arterial remodeling in essential hypertension.