Hypertension, Vol 20, 746-754, Copyright © 1992 by American Heart Association
B Bunkenburg, T van Amelsvoort, H Rogg and JM Wood
This study examines the effects of angiotensin II on hypertrophy and
proliferation of aortic smooth muscle cells from spontaneously hypertensive
and Wistar-Kyoto rats and the receptor subtypes mediating these effects. In
quiescent confluent cells, angiotensin II induced a dose-dependent increase
in thymidine and leucine incorporation without stimulating cell
proliferation. In nonconfluent cells, angiotensin II stimulated cell
proliferation only in combination with a submaximal concentration of fetal
calf serum. These effects were enhanced in cells from spontaneously
hypertensive rats compared with Wistar-Kyoto rats. The effects of
angiotensin II could be blocked by the AT1 receptor antagonist DuP 753 but
not by the AT2 receptor ligand PD 123177. In receptor binding studies with
cells derived from both rat strains, AT1- typical binding was observed.
These data show that the angiotensin II receptors present in vascular
smooth muscle cells in culture from both rat strains are of the AT1
receptor subtype. This receptor subtype appears to mediate vascular smooth
muscle cell hypertrophy and proliferation as well as vasoconstriction.
Although no difference in the receptor profile was detectable between the
two rat strains, the affinity for the ligands to the receptor and the
receptor density tended to be greater in cells from spontaneously
hypertensive rats than in cells from Wistar-Kyoto rats. These results may
partly explain the greater hypotensive response to angiotensin II receptor
blockade in spontaneously hypertensive rats than in Wistar-Kyoto rats,
although both rat strains have the same plasma concentrations of
angiotensin II.
ARTICLES
Receptor-mediated effects of angiotensin II on growth of vascular smooth muscle cells from spontaneously hypertensive rats
Department of Cardiovascular Research, CIBA-GEIGY Ltd., Basel, Switzerland.
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