F Broughton Pipkin, J C Hunter, P M O'Brien, L J Sant-Cassia, S R Turner
{"title":"前列腺素E1和E2对人妊娠中期肾素-血管紧张素系统的影响。","authors":"F Broughton Pipkin, J C Hunter, P M O'Brien, L J Sant-Cassia, S R Turner","doi":"10.3109/10641958309006083","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":79209,"journal":{"name":"Clinical and experimental hypertension. Part B, Hypertension in pregnancy","volume":"2 2","pages":"233-45"},"PeriodicalIF":0.0000,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641958309006083","citationCount":"0","resultStr":"{\"title\":\"Effects on the renin-angiotensin system of the administration of prostaglandin E1 and E2 in second trimester human pregnancy.\",\"authors\":\"F Broughton Pipkin, J C Hunter, P M O'Brien, L J Sant-Cassia, S R Turner\",\"doi\":\"10.3109/10641958309006083\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":79209,\"journal\":{\"name\":\"Clinical and experimental hypertension. Part B, Hypertension in pregnancy\",\"volume\":\"2 2\",\"pages\":\"233-45\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1983-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.3109/10641958309006083\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical and experimental hypertension. Part B, Hypertension in pregnancy\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3109/10641958309006083\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and experimental hypertension. Part B, Hypertension in pregnancy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/10641958309006083","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
我们测量了血浆肾素浓度(PRC)、血浆肾素底物(PRS)和血浆醛固酮浓度(ALD)在输注血管紧张素II (AII)时的诱发变化,同时给予前列腺素E2 5微克min-1 i.v (PGE2)或前列腺素E1 15 ng kg-1 min-1 (PGE1)。实验已在20例患者中使用PGE2,在5例患者中使用PGE1。单独AII (16 ng kg-1 min-1静脉注射)显著降低两组患者的PRC,而不改变PRS,而ALD浓度增加一倍以上。输注PGE2刺激基底PRC;使用剂量的PGE1没有改变PRC。前列腺素没有改变基础RS或ALD浓度。当同时输注AII时,在PGE2存在的情况下,PRC再次受到抑制。然而,当使用PGE1时,只有最小的反馈抑制发生。此外,当与PGE2一起给予AII时,ALD浓度仍然升高两倍以上,但在PGE1存在时,升高幅度要小得多,且不显著。PGE2是一种已知的肾素分泌刺激,明显直接作用于肾小球旁器。这些初步结果表明,尽管在人类妊娠中期存在类似的机制,但PGE1可能具有不同的作用。在PGE1浓度增加的情况下,AII浓度的升高明显阻断了PRC的正常反馈抑制,这一点特别有趣。
Effects on the renin-angiotensin system of the administration of prostaglandin E1 and E2 in second trimester human pregnancy.
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.