Circulation, Vol 87, 283-290, Copyright © 1993 by American Heart Association
H Rakugi, HJ Jacob, JE Krieger, JR Ingelfinger and RE Pratt
BACKGROUND. Angiotensin II promotes growth of vascular smooth muscle cells
in vitro via the autocrine production of growth factors such as
platelet-derived growth factor, basic fibroblast growth factor, and
transforming growth factor-beta. Furthermore, experimental studies have
demonstrated that angiotensin infusion can enhance smooth muscle
proliferation after balloon injury in vivo. Consistent with this,
angiotensin converting enzyme inhibitors have been shown to prevent
myointimal proliferation. The origin of vascular angiotensin that
participate in this process is of interest. We have demonstrated the
presence of angiotensinogen messenger RNA (mRNA) in the adventitial and
medial layers of the rat aorta and have speculated that local
angiotensinogen production may play an important role during myointimal
proliferation. To provide further evidence toward this hypothesis, we
compared the localization and expression of angiotensinogen mRNA in control
and balloon injured vessels using in situ hybridization. METHODS AND
RESULTS. Abdominal aorta of Sprague-Dawley rats were studied before or
after injury with a balloon catheter. Neointimal hyperplasia developed as
documented morphologically by a progressive increase in the ratio of
neointimal to medial thickness from 0.17 at 1 week to 1.17 at 6 weeks after
injury. Angiotensinogen mRNA was detected clearly in the adventitia and
media of control and injured aorta. However, at 1 week after injury, the
medial-to-adventitial angiotensinogen mRNA ratio was higher in the injured
aorta, suggesting increased gene expression in the media compared with
control. Of potential importance, angiotensinogen mRNA was also detected in
the neointima of the injured aorta, and this was also highest at 1 week
after injury. CONCLUSIONS. These data are consistent with the hypothesis
that balloon injury leads to activation of the vascular renin-angiotensin
system, which may participate in the myointimal proliferation.
ARTICLES
Vascular injury induces angiotensinogen gene expression in the media and neointima
Falk Cardiovascular Research Center, Stanford University School of Medicine, Calif 94305-5246.
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