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在对照和肾素分泌增强期间,血管紧张素II在肾脏内的从头生成。

De novo intrarenal formation of angiotensin II during control and enhanced renin secretion.

作者信息

Rosivall L, Narkates A J, Oparil S, Navar L G

出版信息

Am J Physiol. 1987 Jun;252(6 Pt 2):F1118-23. doi: 10.1152/ajprenal.1987.252.6.F1118.

DOI:10.1152/ajprenal.1987.252.6.F1118
PMID:3035944
Abstract

In previous studies it has not been possible to determine net intrarenal formation of angiotensin II (ANG II) from arteriovenous ANG II concentrations because of the high intrarenal ANG II degradation rates (DR). This study was designed to determine ANG II-DR and to estimate net intrarenal ANG II formation during normal and enhanced renin secretion rate (RSR). In anesthetized dogs, plasma renin activity and ANG II were measured in arterial and renal venous blood by radioimmunoassay during four periods: control, renal arterial constriction (RAC), angiotensin converting enzyme (ACE) inhibition (MK 422), and MK 422 plus systemic arterial ANG II infusion. ANG II-DR was determined in each dog from the arterial-renal venous ANG II concentration difference during the period of ANG II infusion in the presence of ACE inhibition; this value was used to estimate net ANG II formation by predicting the amount of arterially delivered ANG II that escaped degradation. The average percent ANG II-DR calculated during ANG II infusion (range of 0.05 to 0.20 microgram/min) was 89 +/- 2%. In response to RAC, RSR increased from 11 +/- 3 to 24 +/- 5 ng ANG I X h-1 X min-1 X g-1. Arterial ANG II (67 +/- 11 pg/ml) and renal venous ANG II (29 +/- 6 pg/ml) increased to 133 +/- 18 and 61 +/- 10 pg/ml, respectively. Net intrarenal ANG II formation increased from 44 +/- 11 to 83 +/- 13 pg X min-1 X g-1 after renal arterial constriction. There was a significant relationship between the change in RSR and the change in ANG II formation rate.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在以往的研究中,由于肾内血管紧张素II(ANG II)降解速率(DR)较高,无法根据动静脉ANG II浓度来确定肾内ANG II的净生成量。本研究旨在测定ANG II-DR,并评估正常和增强肾素分泌速率(RSR)期间肾内ANG II的净生成量。在麻醉犬中,通过放射免疫分析法在四个时期测量动脉血和肾静脉血中的血浆肾素活性和ANG II:对照期、肾动脉收缩(RAC)期、血管紧张素转换酶(ACE)抑制(MK 422)期以及MK 422加全身动脉ANG II输注期。在ACE抑制存在的情况下,根据ANG II输注期动脉-肾静脉ANG II浓度差来确定每只犬的ANG II-DR;该值用于通过预测未降解的动脉输送ANG II量来估计ANG II的净生成量。ANG II输注期间(范围为0.05至0.20微克/分钟)计算出的平均ANG II-DR百分比为89±2%。对RAC的反应中,RSR从11±3增加至24±5纳克ANG I×小时-1×分钟-1×克-1。动脉ANG II(67±11皮克/毫升)和肾静脉ANG II(29±6皮克/毫升)分别增至133±18和61±10皮克/毫升。肾动脉收缩后,肾内ANG II的净生成量从44±11增加至83±13皮克×分钟-1×克-1。RSR的变化与ANG II生成速率的变化之间存在显著关系。(摘要截断于250字)

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