Background: Vascular narrowing in hypertension presents conflicting hypotheses about structural narrowing, vasconstriction, volume expansion, contractile function and other issues more obvious to the physiologist than the cell biologist. Even the cell biology in the injured large arteries used to study atherosclerosis is surprisingly complex. The key issue is that changes in mass, here mainly intimal mass or atherosclerotic plaque, correlate poorly with loss of lumen caliber. An analogy to remodeling of microvessels begs the issue of mechanism.
Recent studies: To explore this, we have focused on two issues: cell death and intramural coagulation. It is likely that cell death, along with tissue factor, promotes coagulation and, in previously injured vessels, fibrin forms in the wall after a repeat injury. In vitro, fibrin promotes smooth muscle gel contraction mediated by an as yet unidentified beta 1 integrin. In vivo, inhibition of coagulation not only prevents vascular narrowing after a reinjury, but may even result in dilation.
Hypothesis: We suggest that injury responses, that is, classical wound contracture mechanisms, can be explained as potential pathways for pathologic vascular remodeling.