(Hypertension. 1999;34:1117-1122.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Effect of Estrogen Replacement on Vasoconstrictor Responses in Rat Mesenteric Arteries
From the Perinatal Research Centre, Departments of Ob/Gyn and Physiology, University of Alberta, Edmonton, Alberta, Canada.
Correspondence to Sandra T. Davidge, PhD, Perinatal Research Centre, 220 HMRC, University of Alberta, Edmonton, Alberta, Canada T6G 2S2. E-mail sandra.davidge{at}ualberta.ca
Abstract—Recent studies have
shown that estrogen can increase endothelial nitric
oxide synthase expression and/or activity and that nitric oxide may
play a role in attenuating vasoconstrictor responses. Yet there are
still controversies in this field. Our hypothesis was that the role of
nitric oxide in modulating vasoconstrictor responses in
estrogen-replaced animals depends on the agonist. The aim of the study
was to determine the effect of long-term estrogen replacement on
vascular reactivity of resistance-sized mesenteric arteries in
ovariectomized rats with the use of a variety of vasoconstrictors.
Female Sprague-Dawley rats were ovariectomized at 11 weeks of age.
17ß-estradiol pellets (0.5 mg/pellet) were implanted in the
estrogen-replaced group (n=9) for 4 weeks; placebo pellets were used in
the ovariectomized group (n=10). Resistance-sized mesenteric arteries
were dissected and mounted onto a dual-chamber arteriograph system.
Estradiol replacement did not alter the response of mesenteric arteries
to either arginine vasopressin or the thromboxane mimetic
U46619. Inhibition of nitric oxide synthase with
NG-monomethyl-L-arginine
(100 µmol/L) did not modulate these vasoconstrictor responses in
either group of rats. In contrast, the dose-response curve of the
adrenergic agonist phenylephrine was significantly
attenuated for the estradiol-replaced rats compared with the
ovariectomized group (EC50=0.90±0.17 vs 0.44±0.08
µmol/L, P<0.05). After incubation with
NG-monomethyl-L-arginine,
the EC50 of phenylephrine significantly
decreased in both groups, but a significant difference remained between
the 2 groups (EC50=0.41±0.08 vs 0.28±0.02 µmol/L,
P<0.05). Importantly, Western
immunoblotting demonstrated that the expression of
1-adrenergic receptors was significantly suppressed by
estradiol replacement. We conclude that estrogen may have a specific
effect on adrenergic vasoconstriction by modulating its receptors.
Key Words: steroids • nitric oxide • receptors, adrenergic, alpha • vasopressin • thromboxanes
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