Bradykinin-induced vasoconstriction and thromboxane release in perfused human placenta.

Bradykinin-induced vasoconstriction and thromboxane release in perfused human placenta.
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灌注人胎盘中缓激肽诱导的血管收缩和血栓素释放。

DOI:
10.1152/ajpendo.1988.254.6.e681
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发表时间:
1988
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Mento,PF
Mento,PF
中科院分区:
--
文献类型:
--
作者:
Wilkes,BM;Mento,PF

文献摘要

被引文献

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本研究旨在研究缓激肽对人胎胎盘循环的影响。向单胎盘子叶动脉灌注RPMI培养基(0.764 ml/min)。缓激肽引起血管阻力的剂量相关增加。由于缓激素通常是一种血管扩张剂,我们研究了缓激素诱导的血管收缩是由于与其他压力系统相互作用的可能性。缓激肽和9,11-二脱氧-9 α,11 α -环氧甲基前列腺素F2 α(一种稳定的血栓素激动剂)引起灌注压的剂量相关性升高。缓激素反应不是由血管紧张素II介导的,因为缓激素诱导的血管收缩不被萨拉拉西(一种竞争性血管紧张素拮抗剂)所抑制。缓激素使血栓素B2的生成增加62.0%。前列腺素E2水平升高86.7%,但对胎盘血管阻力无影响。血管紧张素II不刺激血栓素B2的产生,只引起前列腺素E2的轻微增加。吲哚美辛降低了血管紧张素II的升压反应。SQ29548是一种特异性血栓素拮抗剂,对缓激肽加压反应有61.6%的抑制作用,但没有改变血管紧张素II的反应性。这些数据表明,血栓素是缓激肽诱导的离体人胎盘血管收缩的重要介质。
This investigation was performed to study the effects of bradykinin on the human fetoplacental circulation. The artery to a single placental cotyledon was perfused with RPMI medium (0.764 ml/min). Bradykinin caused a dose-related increase in vascular resistance. Because bradykinin is generally a vasodilator, we investigated the possibility that bradykinin-induced vasoconstriction was due to interactions with other pressor systems. Bradykinin and 9,11-dideoxy-9 alpha, 11 alpha-epoxymethanoprostaglandin F2 alpha (a stable thromboxane agonist) caused a dose-related increase in perfusion pressure. The bradykinin response was not mediated by angiotensin II, because bradykinin-induced vasoconstriction was not inhibited by saralasin, a competitive angiotensin antagonist. Bradykinin increased thromboxane B2 production by 62.0%. Prostaglandin E2 levels were increased by 86.7%, but prostaglandin E2 did not affect fetoplacental vascular resistance. Angiotensin II did not stimulate thromboxane B2 production and caused only a slight increase in prostaglandin E2. Indomethacin decreased the pressor response to angiotensin II. SQ29548, a specific thromboxane antagonist, caused a 61.6% inhibition of the bradykinin pressor response but did not change angiotensin II responsiveness. The data demonstrate that thromboxane is an important mediator of bradykinin-induced vasoconstriction in the isolated perfused human placenta.