Hypertension, Vol 11, 198-207, Copyright © 1988 by American Heart Association
GK Owens, SM Schwartz and M McCanna
The role of smooth muscle cell hypertrophy, hyperploidy, and hyperplasia in
medial hypertrophy of mesenteric resistance vessels of 107- to 111-day-old
spontaneously hypertensive rats (SHR) was examined using a combination of
morphometric, biochemical, and immunological techniques. Mesenteric
arteries were classified on the basis of branching order for comparative
purposes. Branch level I vessels were those that directly enter the jejunal
wall, while Branches II to IV represented more proximal vessels; Branch IV
vessels were those that branch from the superior mesenteric artery. Medial
hypertrophy was assessed in perfusion-fixed vessels by morphometric
evaluation of medial cross-sectional area and smooth muscle content. Medial
cross- sectional area and smooth muscle content were significantly
increased in larger (Branches III and IV) but not smaller (Branches I and
II) mesenteric resistance vessels of SHR compared with control normotensive
Wistar-Kyoto rats (WKY). Smooth muscle cell hypertrophy and hyperploidy
were evaluated in isolated cells obtained by enzymatic dissociation of
mesenteric resistance vessels. Approximately 80% of the cells in these
preparations were identified as smooth muscle cells using a smooth
muscle-specific isoactin antibody. Feulgen-DNA microdensitometric
evaluation of isolated cells showed that polyploid cells were present in
mesenteric resistance vessels but at very low frequencies, and no
differences were apparent between SHR and WKY. Likewise, no differences in
cellular protein content or relative smooth muscle cell size (i.e., area
profile) were observed between cells obtained from SHR and WKY vessels.
These results demonstrate that the increase in medial smooth muscle content
observed in larger mesenteric resistance vessels of SHR cannot be accounted
for by smooth muscle hypertrophy and hyperploidy, inferring that
hyperplasia must be present. Results indicate that studies of the
initiating mechanisms for medial smooth muscle hypertrophy in SHR
resistance vessels, at least relatively early in hypertension, should focus
on examination of factors that induce true cellular proliferation rather
than hypertrophy and hyperploidy.
ARTICLES
Evaluation of medial hypertrophy in resistance vessels of spontaneously hypertensive rats
Department of Physiology, University of Virginia, School of Medicine, Charlottesville 22908.
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