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首页> 外文期刊>American Journal of Physiology >Estrogen potentiates vasopressin-induced contraction of female rat aorta by enhancing cyclooxygenase-2 and thromboxane function.
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Estrogen potentiates vasopressin-induced contraction of female rat aorta by enhancing cyclooxygenase-2 and thromboxane function.

机译：雌激素通过增强环氧合酶2和血栓烷的功能来增强血管加压素诱导的雌性大鼠主动脉收缩。

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摘要

To determine the roles of estrogen and constrictor prostanoids in vasopressin (VP)-induced contraction of female rat aorta, vascular reactivity to VP was determined in thoracic aortas of intact, ovariectomized, and ovariectomized + estrogen-replaced female rats in the presence of indomethacin (Indo), NS-398, SQ-29,548, or vehicle control. The effects of estrogen on vascular reactivity to the thromboxane A(2) analog U-46619 were also examined. Maximal contractile response to VP in intact female rats (5,567 +/- 276 mg/mg of aortic ring wt) was markedly attenuated by ovariectomy (2,485 +/- 394 mg; P < 0.001) and restored by estrogen replacement with 17beta-estradiol (5,059 +/- 194 mg; P > 0.1). Indo and NS-398 significantly attenuated maximal responses to VP in intact female rats to a similar extent [3,176 +/- 179 (P < 0.0001) and 3,258 +/- 152 mg (P < 0.0001), respectively]. Ovariectomy abolished and estrogen replacement restored the inhibitory effects of Indo, NS-398, and SQ-29,548. Contractile responses of rat aorta to U-46619 were significantly greater (P < 0.0001) in females (5,040 +/- 238 mg) than in males (3,679 +/- 96 mg). Ovariectomy markedly attenuated (3,923 +/- 84 mg; P < 0.01) and estrogen replacement restored (5,024 +/- 155 mg; P > 0.1) responses to U-46619 in female aortas. These data reveal that estrogen is an important regulator of the contractile responses of female rat aorta to VP, which appears to potentiate both cyclooxygenase-2 and constrictor prostanoid function in the vascular wall.
机译：为了确定雌激素和缩窄类前列腺素在血管加压素（VP）诱导的雌性大鼠主动脉收缩中的作用，在吲哚美辛存在的情况下，在完整，去卵巢和去卵巢+雌激素替代的雌性大鼠胸主动脉中测定对VP的血管反应性（印度），NS-398，SQ-29,548或车辆控制。还检查了雌激素对血栓烷A（2）类似物U-46619的血管反应性的影响。卵巢切除术（2,485 +/- 394 mg; P <0.001）显着减弱了完整雌性大鼠（5,567 +/- 276 mg / mg的主动脉环重量）对VP的最大收缩反应，并通过用17β-雌二醇替代雌激素来恢复（VP <0.001） 5,059 +/- 194毫克; P> 0.1）。印支和NS-398显着减弱了完整雌性大鼠对VP的最大反应，幅度相似[分别为3,176 +/- 179（P <0.0001）和3,258 +/- 152 mg（P <0.0001）]。卵巢切除术取消，雌激素替代恢复了Indo，NS-398和SQ-29,548的抑制作用。女性（5,040 +/- 238 mg）的大鼠主动脉对U-46619的收缩反应明显大于男性（3,679 +/- 96 mg）（P <0.0001）。卵巢切除术对女性主动脉U-46619的反应明显减弱（3,923 +/- 84 mg; P <0.01），雌激素替代恢复（5,024 +/- 155 mg; P> 0.1）。这些数据表明，雌激素是雌性大鼠主动脉对VP收缩反应的重要调节剂，VP似乎能增强血管壁中的环氧合酶2和收缩型前列腺素功能。

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