Increased sensitivity to angiotensin in uterine arteries from pregnant rabbits.
Increased sensitivity to angiotensin in uterine arteries from pregnant rabbits.
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怀孕兔子宫动脉对血管紧张素的敏感性增加。
DOI：
10.1152/ajpheart.1983.244.3.h335
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Tulenko,T
中科院分区：
文献类型：
--
作者：
Moisey,DM;Tulenko,T
本研究旨在使用分离螺旋条技术比较怀孕（0.92足月）和非怀孕兔子子宫和股动脉平滑肌对血管紧张素 II (ANG II)、去甲肾上腺素 (NE) 和氯化钾 (KCl) 的固有血管反应性。比较剂量反应关系，两组的动脉对 NE 和 KCl 的敏感性相同。然而，怀孕兔的子宫动脉对 ANG II 的血管收缩作用表现出更高的敏感性（P 小于 0.01）。在股动脉中没有观察到这种对 ANG II 敏感性的选择性增加。怀孕兔子子宫动脉中改变的 ANG II 反应不受可卡因或苯氧苯扎明预处理的影响，因此排除了介导该反应的肾上腺素能机制。此外，对子宫动脉 ANG II 受体的萨拉拉辛亲和力 (KB) 的评估表明，它在怀孕期间没有改变。然而，用甲氯芬那酯或吲哚美辛对怀孕兔的子宫动脉进行预孵育，始终会减弱 ANG II 反应（P 小于 0.05）。因此，本研究证明：1）足月妊娠兔的子宫动脉对 ANG II 血管收缩表现出选择性和特异性增强，2）ANG II 的这种反应增强是由于 ANG II 局部刺激子宫动脉壁合成前列腺素，具有净血管收缩作用。
This study was designed to compare the vascular reactivity intrinsic to uterine and femoral arterial smooth muscle from pregnant (0.92 term) and nonpregnant rabbits to angiotensin II (ANG II), norepinephrine (NE), and potassium chloride (KCl) using the isolated helical strip technique. Comparing dose-response relations, arteries from both groups were equally sensitive to NE and KCl. Uterine arteries from pregnant rabbits, however, exhibited a greater sensitivity to the vasoconstricting effects of ANG II (P less than 0.01). This selective increase in sensitivity to ANG II was not observed in femoral arteries. The altered ANG II response in uterine arteries from pregnant rabbits was unaffected by pretreatment with cocaine or phenoxybenzamine, thus ruling out an adrenergic mechanism mediating the response. In addition, evaluation of saralasin affinity (KB) for the uterine arterial ANG II receptor suggested that it was not altered in pregnancy. However, preincubation of uterine arteries from pregnant rabbits with meclofenamate or indomethacin consistently attenuated the ANG II response (P less than 0.05). Therefore, this study demonstrated that 1) uterine arteries from term pregnant rabbits show a selective and specific enhancement to ANG II vasoconstriction, and 2) this increased response of ANG II results from the local ANG II stimulation of synthesis of prostaglandins by the uterine arterial wall that have a net vasoconstricting action.