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利尿剂诱导肾素刺激后尿游离19-去甲-脱氧皮质酮的短暂增加。

Transitory increment in urinary free 19-nor-deoxycorticosterone after diuretic-induced renin stimulation.

作者信息

Griffing G T, Wilson T E, Melby J C

出版信息

J Clin Endocrinol Metab. 1984 Nov;59(5):931-5. doi: 10.1210/jcem-59-5-931.

Abstract

19-Nor-deoxycorticosterone (19-nor-DOC) is a potent mineralocorticoid recently identified in human urine. The factors regulating 19-nor-DOC production are unknown; short term dietary sodium depletion or excess has little effect on 19-nor-DOC excretion in human subjects. This study sought to determine if more prolonged renin stimulation could increase 19-nor-DOC production. Six normal subjects were admitted to a metabolic unit. After a 5-day electrolyte balance period, hydrochlorothiazide (50 mg/day) was administered for 28 days. This treatment resulted in acute natriuresis, a more sustained hypokalemia, and secondary hyperaldosteronism lasting throughout the remainder of the study. Despite the sustained secondary hyperaldosteronism, however, urinary 19-nor-DOC extraction, measured by RIA, increased only slightly on day 3 and subsequently decreased to normal values throughout the remainder of the study (19-nor-DOC, 103 +/- 27 ng/day 0, 175 +/- 26 on day 3, 127 +/- 27 on day 28). The results of this study demonstrate only a minor and transient effect on diuretic-induced renin stimulation on 19-nor-DOC production. Therefore, the physiological regulation of 19-nor-DOC is largely independent of the renin-angiotensin system.

摘要

19-去甲脱氧皮质酮(19-nor-DOC)是最近在人类尿液中发现的一种强效盐皮质激素。调节19-nor-DOC产生的因素尚不清楚;短期饮食中钠的缺乏或过量对人类受试者的19-nor-DOC排泄影响很小。本研究旨在确定更长时间的肾素刺激是否会增加19-nor-DOC的产生。六名正常受试者入住代谢病房。经过5天的电解质平衡期后,给予氢氯噻嗪(50毫克/天),持续28天。这种治疗导致急性利尿、更持久的低钾血症以及在研究的剩余时间内持续的继发性醛固酮增多症。然而,尽管继发性醛固酮增多症持续存在,但通过放射免疫分析法测量的尿19-nor-DOC提取量在第3天仅略有增加,随后在研究的剩余时间内降至正常值(19-nor-DOC,第0天为103±27纳克/天,第3天为175±26纳克/天,第28天为127±27纳克/天)。本研究结果表明,利尿剂诱导的肾素刺激对19-nor-DOC产生的影响仅为轻微且短暂的。因此,19-nor-DOC的生理调节在很大程度上独立于肾素-血管紧张素系统。

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