From the Perinatal Research Centre, Departments of Obstetrics/Gynaecology
and Physiology, University of Alberta, Edmonton, Alberta, Canada (S.T.D.); and
Magee-Womens Research Institute, Departments of Obstetrics, Gynecology &
Reproductive Sciences, University of Pittsburgh (Pa) (J.O., M.K.M.).
Correspondence to Sandra T. Davidge, 220 Heritage Medical Research Centre, University of Alberta, Edmonton, Alberta, Canada T6G 2S2. E-mail sandra.davidge{at}ualberta.ca
Abstract—We tested the hypothesis
that oxidative stress, mediated by dietary vitamin E
deprivation, would alter vascular function through the
interaction of oxygen-derived free radicals and nitric oxide (NO). This
interaction may play an important role in the vascular pathophysiology
of many diseases associated with oxidative stress. Mesenteric arteries
from control (n=12) and vitamin E–deprived (n=12) Sprague-Dawley rats
were studied with a myograph. Superoxide dismutase, which scavenges
superoxide anions, produced a significantly greater relaxation in the
arteries from the vitamin E–deprived rats compared with the controls
(P<.05). Superoxide dismutase and catalase produced
results similar to superoxide dismutase alone. Pretreatment with an NO
synthase inhibitor eliminated the superoxide
dismutase–induced relaxation in arteries from both control and vitamin
E–deprived rats. L-Arginine induced a greater relaxation
in arteries of the vitamin E–deprived group (P<.05).
Agonist-induced relaxation with methacholine was not altered by
superoxide dismutase for either group of animals, indicating that
stimulated release of NO was not influenced by superoxide anions. With
the use of Western immunoblot analysis,
nitrotyrosine residues were shown to be present in arteries from
both the vitamin E–deprived and control rats, but the amount of
nitrotyrosine observed was not different between the two groups. In
summary, our data indicate that there is a greater inhibition of NO
caused by superoxide anions in the vitamin E–deprived group. We
speculate that in conditions of oxidative stress (reduced vitamin E
levels), altered vascular function may be due to increased destruction
of NO by oxygen-derived free radicals.
© 1998 American Heart Association, Inc.
Scientific Contributions
Vascular Function in the Vitamin E–Deprived Rat
An Interaction Between Nitric Oxide and Superoxide Anions
Key Words: endothelium • vitamin E • nitric oxide • superoxide • peroxynitrite • superoxide dismutase
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