Resistance to stretch in human iliac arteries is primarily due to elastin at low pressures, both elastin and collagen at physiological pressures, and almost entirely collagen at high pressures.
The non-linear distensibility of arteries is explained by the sequential mechanical recruitment of elastin at low pressures and collagen at higher physiological pressures.
It is characteristic of arteries that they do not obey Hooke's law, but resist further stretch more strongly, the more they are stretched. It appears that this might be due to the combination of elastin fibers in the elastic laminae, with the much less distensible collagenous libers in the media and adventitia, more and more of which reach their 'unstretched length' as distension is increased. This has been verified on human iliac arteries, from autopsy, by comparing the 'elastic diagrams' (tension vs. circumference) before and after differential digestion of collagen by formic acid, and digestion of elastin by crude trypsin (containing an elastase). This proved that the resistance to stretch at low pressures was almost entirely due to elastin fibers, that at physiological pressures due to both collagenous and elastin fibers, but dominantly to collagen, and that at high pressures almost entirely due to collagenous fibers. In future work on the effect of age on the elasticity of iliac arteries, the initial slope of the elastic diagram can be taken as an index of the state, or number, of the elastin fibers, and the final slope as an index of the state, or number, of collagenous fibers.
Roach et al. (1957) studied Human iliac arteries from autopsy. Differential digestion of collagen and elastin vs. Before digestion was evaluated on Elastic diagrams (tension vs. circumference). Resistance to stretch in human iliac arteries is primarily due to elastin at low pressures, both elastin and collagen at physiological pressures, and almost entirely collagen at high pressures.