Adaptation of resistance arteries to increases in pressure

During the development of hypertension, hypertrophy of smooth muscle cells and deposition of extracellular matrix thicken the walls of large arteries without reducing the size of the lumen. The small arteries and arterioles remodel inwardly through a eutrophic process of rearrangement of the same smooth muscle cells around a smaller lumen. Pressure., through all increase in circumferential wall stress; can account for both hypertrophy and inward entrophic remodeling. The small arteries constrict: curing an elevation of pressure, dins restoring wall stress toward control levels. The large arteries have little vasoactivity and re-stress to the increase in wall stress by initialing a growth process. Mechano-transduction of the pressure stimulus to a growth response is being studied in small mesenteric arteries. Raising the pressure from 90 to 140 mmHg initiates a signaling process starting with phosphorylation of Src within 1 minute. This is followed by phosphorylation of Erk 1/2 peaking at 5 minutes and expression of c-fos mRNA within 30 minutes. Gene expression correlates with wall stress and is thus inhibited by a myogenic response. Maintained vasoconstriction in an isolated arteriole results in inward, eutrophic remodeling within 4 days. Thus the current data support the hypothesis that wall thickness is determined by circumferential wall stress and human size is determined by vascular tone.