FACTORS IMPORTANT IN ARTERIAL NARROWING

Background Vascular narrowing in hypertension presents conflicting hyp otheses about structural narrowing, vasoconstriction, volume expansion , contractile function and other issues more obvious to the physiologi st than the cell biologist Even the cell biology in the injured large arteries used to study atherosclerosis is surprisingly complex. The ke y issue is that changes in mass, here mainly intimal mass or atheroscl erotic plaque, correlate poorly with loss of lumen caliber. An analogy to remodeling of microvessels begs the issue of mechanism. Recent stu dies To explore this, we have focused on two issues: cell death and in tramural coagulation. It is likely that cell death, along with tissue factor, promotes coagulation and, in previously injured vessels, fibri n forms in the wall after a repeat injury. In vitro, fibrin promotes s mooth muscle gel contraction mediated by an as yet unidentified pi int egrin. In vivo, inhibition of coagulation not only prevents vascular n arrowing after a reinjury, but may even result in dilation. Hypothesis We suggest that injury responses, that is, classical wound contractur e mechanisms, can be explained as potential pathways for pathologic va scular remodeling.