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Department of Anesthesiology, Baylor College of Medicine, Houston, Texas 77030
We tested the hypothesis that
endothelium-derived hyperpolarizing factor (EDHF) plays a less dominant
role in the female cerebrovasculature. The contribution of EDHF to the
ATP-mediated dilation was determined in middle cerebral arteries (MCAs)
isolated from male and female rats. Four groups of rats were tested:
intact male (n = 12), intact female (n = 13), estrogen-treated ovariectomized female (n = 13), and vehicle-treated ovariectomized female (n = 20)
rats. Maximal dilation to ATP was similar in all groups. However, in
the presence of
N
-nitro-L-arginine methyl ester
(L-NAME, 3 × 10
5 M) and indomethacin
(105 M), the maximal dilation to ATP was significantly
reduced in intact female (24 ± 9%) and estrogen-treated
ovariectomized female (29 ± 9%) rats compared with intact male
(95 ± 4%) and vehicle-treated ovariectomized female (96 ± 2%) rats. The ATP-mediated dilation in L-NAME- and
indomethacin-treated MCAs isolated from male and ovariectomized female
rats was inhibited by charybdotoxin (107 M), an inhibitor
of large-conductance Ca2+-sensitive K+
channels. We have defined EDHF as the L-NAME- and
indomethacin-insensitive component of the ATP-mediated dilation. Our
findings indicate that EDHF-mediated dilations are negligible in the
female rat MCA; these dilations can be significantly enhanced after
ovariectomy, suggesting that this effect is mediated by estrogen.
gender; vascular
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