Hypertension, Vol 22, 665-676, Copyright © 1993 by American Heart Association
F Contard, A Sabri, M Glukhova, S Sartore, F Marotte, JP Pomies, P Schiavi, D Guez, JL Samuel and L Rappaport
The aim of this study was to determine the phenotype of smooth muscle cells
in the arteries of chronically hypertensive animals and to analyze the
effects of treatments known to increase the survival of the animal without
a clear effect on its hypertensive state. Stroke-prone spontaneously
hypertensive rats (SHRSP) kept on a 1% sodium drinking solution were
untreated or treated with one of two diuretics, indapamide (3 mg/kg per
day) or hydrochlorothiazide (20 mg/kg per day), from 6 to 13 weeks of age.
Phenotype was characterized by the immunolabeling of arteries with
antibodies raised against a cellular form (EIIIA) of fibronectin,
alpha-smooth muscle actin, and nonmuscle myosin. We demonstrated that
phenotypes of smooth muscle cells of the SHRSP differ from those found in
Wistar-Kyoto rats. The difference in phenotype is specific for the vessel
type: ie, an increased expression of nonmuscle myosin in the aorta and of
both EIIIA fibronectin and nonmuscle myosin in the coronary arteries. The
two diuretics (1) had no effect on blood pressure, (2) prevented or did not
prevent the increase in medial thickness, and (3) prevented changes in both
smooth muscle cell phenotype and ischemic tissular lesions. Taken together,
the results suggest that in SHRSP the changes in the phenotype of smooth
muscle cells and the thickness of arteries are unrelated events. We propose
that the maintenance of the contractile phenotype of the arterial smooth
muscle cells could be an essential parameter involved in the prevention of
the deleterious consequences characteristic of a severe hypertensive state.
ARTICLES
Arterial smooth muscle cell phenotype in stroke-prone spontaneously hypertensive rats
U127 INSERM, Hopital Lariboisiere, Paris, France.
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