(Hypertension. 1997;29:1351-1356.)
© 1997 American Heart Association, Inc.
Articles |
Estrogen Maintains Nitric Oxide Synthesis in Arterioles of Female Hypertensive Rats
From the Department of Physiology, New York Medical College, Valhalla.
Correspondence to Akos Koller, MD, PhD, Department of Physiology, New York Medical College, Valhalla, NY 10595.
Abstract We hypothesized that in female spontaneously
hypertensive rats (SHR), estrogen moderates the dysfunction of
arterioles by preserving nitric oxide synthesis. To this end, we
conducted experiments on isolated gracilis muscle arterioles
(approximately 55 µm in diameter) of 12-week-old SHR divided
into four groups: females (fSHR), ovariectomized females (fSHR-OV),
ovariectomized females with estrogen replacement (fSHR-OV+ES, 50
µg/kg SC 17ß-estradiol benzoate every 48 hours), and males (mSHR).
Arteriolar diameter in the presence of perfusion pressures of 60, 80,
100, and 120 mm Hg were obtained, and diameter changes were
measured (at 80 mm Hg) in response to various concentrations of
substance P (10-9 to
5x10-8 mol/L), sodium nitroprusside
(10-8 to 10-6 mol/L),
and A23187 (5x10-8 to
10-6 mol/L). The pressure-induced diameter of
mSHR and fSHR-OV arterioles was significantly less (by approximately
10%) than that of fSHR and fSHR-OV+ES arterioles.
N
-nitro-L-arginine
(10-4 mol/L), a nitric oxide synthase
inhibitor, elicited a significant decrease in basal
arteriolar diameter of fSHR (by approximately 19%) and fSHR-OV+ES (by
approximately 17%), thereby eliminating the differences in tone among
the various groups. Dilations of fSHR and fSHR-OV+ES arterioles to
substance P were significantly greater (by 140% at a concentration of
5x10-8 mol/L) than those of mSHR and fSHR-OV
arterioles, whereas dilations to sodium nitroprusside were not
different among the groups. A23187 (a nitric oxide releaser) elicited
dilations in arterioles of fSHR (5.9±1.5%, 13.0±1.8%, and
19.2±2.1%) and fSHR-OV+ES (4.3±1.0%, 10.3±2.4%, and 15.0±4.0%)
but constrictions in those of mSHR (-7.5±1.6%, -25.3±39%, and
-36.9±4.1%) and fSHR-OV (-2.6±1.7%, -7.4±3.3%, and
-11.5±6.1%). We conclude that estrogen in fSHR is responsible for
the preservation of nitric oxide synthesis in skeletal muscle
arterioles, resulting in a greater modulation of pressure-induced
myogenic tone than in mSHR and maintenance of nitric
oxide–mediated dilations.
Key Words: estradiol • arterioles • rats, inbred SHR • nitric oxide
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