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Hypertension, Vol 18, 748-757, Copyright © 1991 by American Heart Association
AF Dominiczak, DF Lazar, AK Das and DF Bohr
Membrane microviscosity, phospholipid composition, and turnover were
measured in cultured vascular smooth muscle cells isolated from mesenteric
arteries of stroke-prone spontaneously hypertensive and age- matched,
normotensive Wistar-Kyoto rats. Membrane microviscosity, measured with
fluorescence polarization, revealed greater microviscosity (lower fluidity)
of the membranes isolated from smooth muscle cells from hypertensive as
compared with those isolated from normotensive rats (p less than 0.01).
Preincubation of membranes from hypertensive rats with 5 mM calcium reduced
membrane microviscosity in "core" and in "surface" regions of the bilayer
toward values observed in Wistar-Kyoto rats. Phospholipid composition did
not differ between intact aortas and cultured mesenteric cells or between
those tissues obtained from normotensive and from hypertensive rats. The
total lipid- associated radioactivity was significantly lower in cells from
stroke- prone spontaneously hypertensive rats than in those from
Wistar-Kyoto controls (p less than 0.01). Phosphatidylcholine incorporated
70% and phosphatidylinositol 16% of total lipid-associated radioactivity,
with no difference between cells from hypertensive and normotensive
animals. Turnover of phosphatidylethanolamine was greater in cells from
Wistar- Kyoto rats (p = 0.02), whereas turnover of phosphatidylserine was
greater in cells from stroke-prone spontaneously hypertensive rats (p =
0.04). The greater microviscosity of the lipid bilayer in hypertension is a
generalized defect of the matrix in which the transport proteins function.
We hypothesize that this defect is responsible for the multiple
abnormalities of membrane transport systems that have been described in
genetic hypertension.
ARTICLES
Lipid bilayer in genetic hypertension
Department of Physiology, University of Michigan, Ann Arbor.
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