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妊娠中期给予前列腺素E1和E2对人肾素-血管紧张素系统的影响。

Effects on the renin-angiotensin system of the administration of prostaglandin E1 and E2 in second trimester human pregnancy.

作者信息

Broughton Pipkin F, Hunter J C, O'Brien P M, Sant-Cassia L J, Turner S R

出版信息

Clin Exp Hypertens B. 1983;2(2):233-45. doi: 10.3109/10641958309006083.

Abstract

We have measured evoked changes in plasma renin concentration (PRC), plasma renin substrate (PRS) amd plasma aldosterone concentration (ALD) during the infusion of angiotensin II (AII) with and without the simultaneous administration of prostaglandin E2, 5 micrograms min-1 i.v. (PGE2) or prostaglandin E1, 15 ng kg-1 min-1 (PGE1). Experiments have been carried out using PGE2 in 20 patients, and in 5 patients to date with PGE1. AII alone (16 ng kg-1 min-1 i.v.) significantly reduced PRC in both groups of patients without altering PRS, while ALD concentrations more than doubled. The infusion of PGE2 stimulated basal PRC; PGE1 at the dose used did not alter PRC. Neither prostaglandin altered basal RS or ALD concentrations. When AII was infused simultaneously, PRC was again suppressed, in the presence of PGE2. However, only minimal feedback suppression occurred when PGE1 was being used. Furthermore, AII was still associated with a more than two-fold rise in ALD concentration when given together with PGE2, but the rise was considerably smaller and not significant in the presence of PGE1. PGE2 is a known stimulus to renin secretion, apparently acting directly at the juxtaglomerular apparatus. These preliminary results suggest that while a similar mechanism exists in second trimester human pregnancy, PGE1 may have a different effect. The apparent blockade of the normal feedback suppression of PRC in the presence of increased PGE1 concentrations by raised concentrations of AII is especially interesting.

摘要

我们已经测量了在静脉输注血管紧张素II(AII)期间,血浆肾素浓度(PRC)、血浆肾素底物(PRS)和血浆醛固酮浓度(ALD)的诱发变化,同时给予或不给予前列腺素E2(5微克/分钟静脉注射,PGE2)或前列腺素E1(15纳克/千克/分钟,PGE1)。已对20例患者使用PGE2进行了实验,迄今为止对5例患者使用了PGE1。单独输注AII(16纳克/千克/分钟静脉注射)可显著降低两组患者的PRC,而不改变PRS,同时ALD浓度增加了一倍多。输注PGE2可刺激基础PRC;所用剂量的PGE1未改变PRC。两种前列腺素均未改变基础RS或ALD浓度。同时输注AII时,在PGE2存在的情况下,PRC再次受到抑制。然而,使用PGE1时仅出现最小程度的反馈抑制。此外,AII与PGE2一起给药时,ALD浓度仍会有两倍以上的升高,但在PGE1存在的情况下,升高幅度明显较小且无统计学意义。PGE2是肾素分泌的已知刺激物,显然直接作用于肾小球旁器。这些初步结果表明,虽然在妊娠中期的人类中存在类似机制,但PGE1可能具有不同的作用。在PGE1浓度升高的情况下,AII浓度升高对PRC正常反馈抑制的明显阻断尤其令人感兴趣。

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