The effect of ACTH and cortisol on aldosterone and cortisol clearance and distribution in plasma and whole blood.

The effect of ACTH and cortisol on aldosterone and cortisol clearance and distribution in plasma and whole blood.
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ACTH 和皮质醇对血浆和全血中醛固酮和皮质醇清除率和分布的影响。

DOI:
10.1210/jcem-43-5-1101
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发表时间:
1976
期刊:
The Journal of clinical endocrinology and metabolism
影响因子:
--
通讯作者:
R. Horton
R. Horton
中科院分区:
--
文献类型:
--
作者:
R. Zipser;P. Speckart;P. Zia;W. Edmiston;F. Y. Lau;R. Horton

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在13名接受心导管检查的受试者和9名健康对照者中研究了ACTH或皮质醇给药后醛固酮和皮质醇代谢清除率(MCR)增加的机制。在对照受试者中,两种类固醇的MCR(血浆)均增加29%(醛固酮:936 +/- 57至1204 +/- 55 l/天/m2,皮质醇:从205 +/- 12到264 +/- 17 l/day/m2 +/- SE),皮质醇(12 mg/h)给药1到2 h后分别降低20和32%。相比之下,醛固酮MCR(全血)不随ACTH或皮质醇给药而变化(从1276 +/- 57至1330 +/- 59 l/天/m2),表明血浆MCR增加是由于醛固酮从血浆重新分配至红细胞所致。早晨皮质醇水平正常时,醛固酮内脏提取率为92 +/- 1%(n = 12),ACTH给药后提取率无变化。然而,对于皮质醇,在给予ACTH或皮质醇后,内脏提取物从8 +/- 0.8%增加到17.8 +/-5.0%,MCR(全血)同样增加了15 - 31%(从295 +/- 23增加到357 +/- 30 l/天/m2)。血浆和红细胞中示踪剂醛固酮浓度的体内和体外测量(在37 ℃)显示,随着皮质醇浓度的增加,分布到红细胞中的增加。结果表明,一部分醛固酮结合在血浆中,并被皮质醇置换到红细胞中。血浆醛固酮MCR增加,但全血MCR不变,因为肝脏几乎完全从血浆和红细胞中提取醛固酮。皮质醇MCR(血浆)的增加是由于血浆结合位点接近饱和时内脏提取增加和重新分布到红细胞中所致。
The mechanisms of increased aldosterone and cortisol metabolic clearance rates (MCR) following ACTH or cortisol administration were studied in 13 subjects undergoing cardiac catheterization and in 9 healthy controls. In control subjects, the MCR (plasma) of both steroids increased by 29% (aldosterone: from 936 +/- 57 to 1204 +/- 55 l/day/m2, cortisol: from 205 +/- 12 to 264 +/- 17 l/day/m2 +/- SE) after ACTH (12 units/h) for 1 to 4 h, and by 20 and 32%, respectively, after cortisol (12 mg/h) for 1 to 2 h. In contrast, aldosterone MCR (whole blood) did not change with ACTH or cortisol administration (from 1276 +/- 57 to 1330 +/- 59 l/day/m2), indicating that the plasma MCR increase results from a redistribution of aldosterone from plasma to red cells. Aldosterone splanchnic extraction was 92 +/- 1% (n = 12) with normal morning cortisol levels, and extraction was unchanged after ACTH administration. For cortisol, however, the splanchnic extraction increased from 8 +/- 0.8% to 17.8 +/- 5.0%, and the MCR (whole blood) likewise increased by 15 to 31% (from 295 +/- 23 to 357 +/- 30 l/day/m2), after ACTH or cortisol administration. In vivo and in vitro measurements (at 37 C) of tracer aldosterone concentration in plasma and in red cells showed an increase in distribution to red cells with increasing cortisol concentrations. The results suggest that a fraction of aldosterone is bound in plasma and displaced by cortisol into red cells. There is an increased aldosterone plasma MCR, but unaltered whole blood MCR, since the liver extracts aldosterone almost completely from both plasma and red cells. The increase in cortisol MCR (plasma) results from both an increased splanchnic extraction as plasma binding sites approach saturation and a redistribution into red cells.