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大鼠肾上腺素代谢途径的个体发生:糖皮质激素的作用。

Ontogeny of epinephrine metabolic pathways in the rat: role of glucocorticoids.

作者信息

Kennedy B, Ziegler M G

机构信息

Department of Medicine, University of California San Diego, Medical Center, 200 West Arbor Drive, 8341, San Diego, CA, USA.

出版信息

Int J Dev Neurosci. 2000 Feb;18(1):53-9. doi: 10.1016/s0736-5748(99)00106-9.

DOI:10.1016/s0736-5748(99)00106-9
PMID:10708906
Abstract

Recent studies suggest that the initial expression of adrenal phenylethanolamine N-methyltransferase (PNMT) and epinephrine (E) are dependent upon stimulation of adrenal glucocorticoid receptors. However, evidence suggests that the expression of heart and brain PNMT is independent of glucocorticoids. We measured PNMT activity and E levels in adrenal, heart and head over the latter half of gestation in rat fetuses treated chronically with glucocorticoids, and in normal controls. Chronic glucocorticoid treatment ending on embryonic day (e)12 did not affect heart, head or trunk PNMT activity or E levels. In contrast, chronic glucocorticoid exposure ending e19 or e20 resulted in marked increases in both PNMT and E in adrenal, heart and head tissues. The elevation of E in all three tissues was unaffected by maternal adrenalectomy, indicating enhanced fetal E synthesis. In the absence of exogenous glucocorticoid treatment heart PNMT activity peaked on e12, prior to the earliest reported appearance of glucocorticoid receptors. We conclude that expression of PNMT in all three tissues is glucocorticoid independent until the latter part of gestation when it is readily enhanced by glucocorticoids.

摘要

近期研究表明,肾上腺苯乙醇胺N - 甲基转移酶(PNMT)和肾上腺素(E)的初始表达依赖于肾上腺糖皮质激素受体的刺激。然而,有证据表明心脏和脑PNMT的表达与糖皮质激素无关。我们测定了长期接受糖皮质激素治疗的大鼠胎儿以及正常对照胎儿在妊娠后半期肾上腺、心脏和头部的PNMT活性及E水平。在胚胎第(e)12天结束的慢性糖皮质激素治疗并未影响心脏、头部或躯干的PNMT活性及E水平。相比之下,在e19或e20结束的慢性糖皮质激素暴露导致肾上腺、心脏和头部组织中PNMT和E均显著增加。所有三个组织中E的升高不受母体肾上腺切除术的影响,表明胎儿E合成增强。在无外源性糖皮质激素治疗的情况下,心脏PNMT活性在e12达到峰值,早于最早报道的糖皮质激素受体出现时间。我们得出结论,在妊娠后期糖皮质激素易使其增强之前,所有三个组织中PNMT的表达均不依赖于糖皮质激素。

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