A hallmark of vascular disease is the inappropriate proliferative and
synthetic behaviour of vascular smooth muscle cells. This phenotypical
ly immature behaviour arises as a consequence of the myocytes undergoi
ng phenotypic conversion and/or clonal proliferation of a ''fetal'' ty
pe of smooth muscle cell preexisting in the vessel wall. De-differenti
ation and initiation of proliferation is not only induced by endotheli
al desquamation and acute exposure of smooth muscle cells to platelet-
derived mitogens, but also occurs in the uninjured blood vessel. There
fore normal components of the blood vessel are implicit in the patholo
gical process. These include vasoconstrictor peptides, growth factor p
eptides and extracellular matrix molecules. In vitro and in vivo exper
imentation has indicated that while some of these compounds individual
ly are only mild stimulators of smooth muscle proliferative metabolism
, they may act synergistically to induce robust responses. Here we dis
cuss the effects of the vasoconstrictor peptide angiotensin II, which
can be locally generated within the vessel wall itself, on the express
ion of extracellular matrix molecules in vitro and in vivo. We focus o
n the angiotensin II-modulated expression of extracellular matrix glyc
oproteins, e.g. thrombospondin, tenascin, fibronectin and laminin.