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Department of Physiology, New York Medical College, Valhalla, New York 10595
To investigate the role of estrogen in
flow-induced dilation (FiD) in nitric oxide (NO) deficiency, FiD was
examined in isolated gracilis arterioles of ovariectomized
(OVX) and OVX rats with estrogen replacement (OVE). Both groups
of rats were treated chronically with
N
-nitro-L-arginine methyl ester.
Plasma concentration of NO2/NO3 was reduced in
both groups. Plasma concentration of estradiol was lower in OVX than in
OVE rats. FiD was similar in vessels of the two groups; calculated wall
shear stress and basal tone were significantly greater in OVX vs. OVE
rats. Indomethacin did not affect FiD in vessels from OVE rats but
abolished dilation in vessels from OVX rats. Valeryl salicylate or
NS-398 inhibited FiD by ~50%, whereas their simultaneous
administration eliminated the response in arterioles from OVX rats. In
vessels from OVE rats, miconazole or charybdotoxin eliminated FiD.
Thus, in NO deficiency, prostaglandins derived from both cyclooxygenase
isoforms mediate FiD in gracilis arterioles of OVX rats. Estrogen
replacement switches the mediation, showing dependence on
endothelium-derived hyperpolarizing factor in the
arterioles of OVE rats.
ovariectomy; estrogen replacement; potassium channels; arterioles; endothelium-derived hyperpolarizing factor; nitric oxide
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