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首页> 外文期刊>American Journal of Physiology >Role of estrogen in modulating EDHF-mediated dilations in the female rat middle cerebral artery.
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Role of estrogen in modulating EDHF-mediated dilations in the female rat middle cerebral artery.

机译：雌激素在雌性大鼠大脑中动脉调节EDHF介导的扩张中的作用。

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摘要

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(omega)-nitro-L-arginine methyl ester (L-NAME, 3 x 10(-5) M) and indomethacin (10(-5) 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 (10(-7) 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.
机译：我们测试了这一假设，即内皮源性超极化因子（EDHF）在女性脑血管系统中的作用较小。在从雄性和雌性大鼠中分离出的中脑动脉（MCA）中确定了EDHF对ATP介导的扩张的贡献。测试了四组大鼠：完整的雄性（n = 12），完整的雌性（n = 13），经雌激素处理的去卵巢雌性大鼠（n = 13）和经媒介物处理的去卵巢雌性大鼠（n = 20）。在所有组中对ATP的最大扩张相似。但是，在存在N（ω）-硝基-L-精氨酸甲酯（L-NAME，3 x 10（-5）M）和消炎痛（10（-5）M）的情况下，最大的ATP扩张显着与完整雄性（95 +/- 4％）和媒介物处理过的雌性卵巢切除雌性（96 +/-）相比，完整雌性（24 +/- 9％）和经雌激素治疗的去卵巢雌性（29 +/- 9％）大鼠减少2％）大鼠。沙丁毒素（10（-7）M）是大传导性Ca2 +敏感的K +通道的抑制剂，可抑制从雄性和去卵巢的雌性大鼠中分离得到的L-NAME和消炎痛治疗的MCA中的ATP介导的扩张。我们将EDHF定义为ATP介导的扩张反应的L-NAME和吲哚美辛不敏感成分。我们的发现表明，在雌性大鼠MCA中，EDHF介导的扩张作用可忽略不计。这些切除可以在卵巢切除术后显着增强，表明这种作用是由雌激素介​​导的。

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