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首页> 外文期刊>American Journal of Physiology >Chronic stress induces adrenal hyperplasia and hypertrophy in a subregion-specific manner.
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Chronic stress induces adrenal hyperplasia and hypertrophy in a subregion-specific manner.

机译：慢性应激以亚区域特异性方式诱导肾上腺增生和肥大。

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The adrenal gland is an essential stress-responsive organ that is part of both the hypothalamic-pituitary-adrenal axis and the sympatho-adrenomedullary system. Chronic stress exposure commonly increases adrenal weight, but it is not known to what extent this growth is due to cellular hyperplasia or hypertrophy and whether it is subregion specific. Moreover, it is not clear whether increased production of adrenal glucocorticoid after chronic stress is due to increased sensitivity to adrenocorticotropic hormone (ACTH) vs. increased maximal output. The present studies use a 14-day chronic variable stress (CVS) paradigm in adult male rats to assess the effects of chronic stress on adrenal growth and corticosterone steroidogenesis. Exogenous ACTH administration (0-895 ng/100 g body wt) to dexamethasone-blocked rats demonstrated that CVS increased maximal plasma and adrenal corticosterone responses to ACTH without affecting sensitivity. This enhanced function was associated with increased adrenal weight, DNAand RNA content, and RNA/DNA ratio after CVS, suggesting that both cellular hyperplasia and hypertrophy occurred. Unbiased stereological counting of cells labeled for Ki67 (cell division marker) or 4,6-diamidino-2-phenylindole (nuclear marker), combined with zone specific markers, showed that CVS induced hyperplasia in the outer zona fasciculata, hypertrophy in the inner zona fasciculata and medulla, and reduced cell size in the zona glomerulosa. Collectively, these results demonstrate that increased adrenal weight after CVS is due to hyperplasia and hypertrophy that occur in specific adrenal subregions and is associated with increased maximal corticosterone responses to ACTH. These chronic stress-induced changes in adrenal growth and function may have implications for patients with stress-related disorders.
机译：肾上腺是重​​要的应激反应器官，是下丘脑-垂体-肾上腺轴和交感-肾上腺髓质系统的一部分。慢性应激暴露通常会增加肾上腺重量，但尚不清楚这种增长在多大程度上是由于细胞增生或肥大引起的，以及是否是亚区域特异性的。此外，尚不清楚慢性应激后肾上腺糖皮质激素的产生增加是否是由于对肾上腺促皮质激素（ACTH）的敏感性相对于最大产量的增加。本研究使用成年雄性大鼠的14天慢性可变应激（CVS）范例来评估慢性应激对肾上腺生长和皮质酮类固醇生成的影响。地塞米松阻断大鼠的外源ACTH给药（0-895 ng / 100 g体重）表明CVS增加了血浆和肾上腺皮质激素对ACTH的最大反应，而不会影响敏感性。这种增强的功能与CVS后肾上腺重量，DNA和RNA含量以及RNA / DNA比例增加有关，提示细胞增生和肥大都会发生。对标记为Ki67（细胞分裂标记）或4,6-二mid基-2-苯基吲哚（核标记）的细胞进行无偏见的立体计数，结合区域特异性标记，表明CVS诱导了筋膜外增生，内膜增生筋膜和延髓，并降低了肾小球带状细胞的大小。总的来说，这些结果表明，CVS后肾上腺重量增加是由于发生在特定肾上腺局部区域的增生和肥大，并且与最大皮质酮对ACTH的反应增加有关。这些慢性应激诱导的肾上腺生长和功能变化可能对患有应激相关疾病的患者产生影响。

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