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首页> 外文期刊>American Journal of Physiology >Estrogen increases iNOS expression in the ovine coronary artery.
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Estrogen increases iNOS expression in the ovine coronary artery.

机译：雌激素可增加绵羊冠状动脉中iNOS的表达。

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Estrogen is believed to protect postmenopausal women from coronary vascular disease, in part by increasing production of nitric oxide (NO). In this study, we investigated the possibility that transcriptional activation of inducible NO synthase (iNOS) is responsible for a component of the estrogen-induced increase in coronary blood flow. Twenty-two ewes were instrumented with Doppler flow probes on their left circumflex coronary and pulmonary arteries. Nine ewes received 17beta-estradiol (1 microg/kg), and the coronary vascular response was followed for 16 h. Estradiol significantly increased coronary blood flow by 22 +/- 4% over baseline and the peak response occurred at 2 h (P < 0.01). To examine the effect of estrogen on NOS expression in the ovine coronary artery, 17 noninstrumented animals were killed 2 h after administration of estradiol or vehicle. Coronary arteries were analyzed for ovine iNOS and endothelial NOS (eNOS) expression by semiquantitative RT-PCR. PCR primers were based on partial cDNA clones for ovine eNOS and iNOS isolated as part of this study. The expression of iNOS was significantly increased (27-fold) by the administration of estradiol, whereas the expression of eNOS was much weaker (2-fold). To confirm these effects in vivo, additional instrumented animals received either the estrogen receptor (ER) antagonist ICI-182,780 (n = 5), the iNOS antagonist dexamethasone (n = 5), or pyrrolidine dithiocarbamic acid, an inhibitor of nuclear factor-kappaB (n = 5). All three antagonists inhibited estrogen-induced increases in coronary blood flow and increases in cardiac output by over 85%. These results strongly support the hypothesis that 17beta-estradiol increases coronary blood flow in the unanesthetized nonpregnant ewe via an ER-dependent mechanism that results in an increase in both eNOS and iNOS expression.
机译：据信雌激素可保护绝经后妇女免于冠状血管疾病，部分原因是通过增加一氧化氮（NO）的产生。在这项研究中，我们调查了诱导型一氧化氮合酶（iNOS）转录激活是由雌激素引起的冠状动脉血流增加的原因。 22只母羊的左旋支冠状动脉和肺动脉上装有多普勒血流探头。九只母羊接受17β-雌二醇（1微克/千克），并跟踪冠状动脉反应16小时。雌二醇比基线显着增加了冠状​​动脉血流量22 +/- 4％，并且峰值反应发生在2 h（P <0.01）。为了检查雌激素对绵羊冠状动脉NOS表达的影响，在给予雌二醇或媒介物2小时后杀死了17只非仪表动物。通过半定量RT-PCR分析冠状动脉的绵羊iNOS和内皮NOS（eNOS）表达。 PCR引物基于绵羊eNOS和iNOS的部分cDNA克隆，这是本研究的一部分。通过雌二醇给药，iNOS的表达显着增加（27倍），而eNOS的表达则弱得多（2倍）。为了在体内确认这些作用，另外的有仪器动物接受了雌激素受体（ER）拮抗剂ICI-182,780（n = 5），iNOS拮抗剂地塞米松（n = 5）或吡咯烷二硫代氨基甲酸（一种核因子-κB抑制剂） （n = 5）。所有这三种拮抗剂均抑制雌激素诱导的冠状动脉血流量增加，并使心输出量增加超过85％。这些结果有力地支持了17β-雌二醇通过ER依赖性机制增加eNOS和iNOS表达均增加的未麻醉非怀孕母羊中冠状动脉血流量的假设。

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