Hypertension, Vol 17, 902-908, Copyright © 1991 by American Heart Association
F Hansen-Smith, AS Greene, AW Cowley Jr, L Lougee and JH Lombard
Loss of microvessels (anatomic rarefaction) occurs in chronic reduced renal
mass (RRM) hypertension and is mediated via structural degeneration of
vascular smooth muscle (VSM) and endothelial cells. The purpose of the
present study was to determine if structural changes occur in VSM cells of
the microvessels that remain in the tissue of rats with chronic RRM
hypertension. Samples of cremaster muscles were taken from normotensive
control rats and rats with acute (3-7 days) and chronic (14-28 days) RRM
hypertension (75% reduction in kidney mass with 4% NaCl loading). The
samples were fixed in situ and processed for light and electron microscopy.
Ultrastructural morphology of VSM cells in terminal arterioles of control
animals was normal. Although VSM morphology in many microvessels of RRM
hypertensive rats was also normal, some vessels exhibited structural
changes that were not present in arterioles of the normotensive animals.
The most striking change was the appearance of more extensive dense bodies
anchoring the contractile filaments around the outer membrane of the cells.
Extreme vasoconstriction was observed in some arterioles of RRM rats as
long as 2 weeks after salt loading. Focal areas of VSM cell proliferation
were evident. Many of the changes occurring in RRM were detected as early
as 1 week after the onset of hypertension. These observations suggest that
renal mass reduction-salt loading hypertension is associated with early
structural and functional changes in the VSM cells.
ARTICLES
Structural alterations of microvascular smooth muscle cells in reduced renal mass hypertension
Department of Biological Sciences, Oakland University, Rochester, Mich.
This article has been cited by other articles:
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F. M. Hansen-Smith, L. W. Morris, A. S. Greene, and J. H. Lombard Rapid Microvessel Rarefaction With Elevated Salt Intake and Reduced Renal Mass Hypertension in Rats Circ. Res., August 1, 1996; 79(2): 324 - 330. [Abstract] [Full Text] |
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