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血管紧张素II和钾对18-羟基-11-脱氧皮质酮分泌的刺激作用。

Stimulation of 18-hydroxy-11-deoxycorticosterone secretion by angiotensin II and potassium.

作者信息

Moore T J, Braley L M, Williams G H

出版信息

Endocrinology. 1978 Jul;103(1):152-5. doi: 10.1210/endo-103-1-152.

DOI:10.1210/endo-103-1-152
PMID:744066
Abstract

The control of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) secretion is incompletely understood: ACTH seems to be the dominant regulator, the importance of angiotensin II (A-II) is uncertain, and the effect of potassium has not been investigated. The purpose of this study was to evaluate the 18-OH-DOC response to these three stimuli in vitro. Suspensions of isolated rat adrenal glomerulosa or fasciculata cells were stimulated with either alpha-1-24 ACTH (0.04 mU/ml), A-II (25 ng/ml), or potassium (5.9 mEq/liter), and 18-OH-DOC production was measured. In glomerulosa cells, ACTH produced the greatest 18-OH-DOC response but A-II and potassium also produced significant (P less than 0.001) 18-OH-DOC increases (control, 162 +/- 14 (SE) ng/10(6) cells incubated; A-II, 368 +/- 39; potassium, 380 +/- 37; ACTH, 1544 +/- 165). In fasciculata cells, 18-OH-DOC production increased with ACTH but not with A-II or potassium. These results document that A-II and potassium, as well as ACTH, can stimulate 18-OH-DOC production by glomerulosa but not by fascicuata cells. The response to A-II may provide an explanation for the reported increase in 18-OH-DOC production after sodium restriction.

摘要

18-羟-11-脱氧皮质酮(18-OH-DOC)分泌的调控机制尚未完全明确:促肾上腺皮质激素(ACTH)似乎是主要调节因子,血管紧张素II(A-II)的作用尚不明确,钾的影响也未得到研究。本研究旨在评估体外条件下这三种刺激对18-OH-DOC的反应。分离的大鼠肾上腺球状带或束状带细胞悬液分别用α-1-24 ACTH(0.04 mU/ml)、A-II(25 ng/ml)或钾(5.9 mEq/升)刺激,然后测定18-OH-DOC的生成量。在球状带细胞中,ACTH引起的18-OH-DOC反应最大,但A-II和钾也能显著(P<0.001)增加18-OH-DOC的生成量(对照组,每10⁶个孵育细胞中为162±14(SE)ng;A-II组,368±39;钾组,380±37;ACTH组,1544±165)。在束状带细胞中,18-OH-DOC的生成量随ACTH增加,但不随A-II或钾增加。这些结果表明,A-II、钾以及ACTH均可刺激球状带细胞生成18-OH-DOC,但不能刺激束状带细胞。对A-II的反应可能解释了钠限制后报道的18-OH-DOC生成量增加的现象。

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