Splanchnicotomy increases adrenal sensitivity to ACTH in nonstressed rats
Splanchnicotomy increases adrenal sensitivity to ACTH in nonstressed rats
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DOI：
10.1152/ajpendo.1997.273.2.e363
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发表时间：
1997-08-01
影响因子：
5.1
通讯作者：
Engeland, WC
中科院分区：
文献类型：
--
作者：
Jasper, MS;Engeland, WC
醒着的大鼠肾上腺皮质酮分泌有超昼夜节律。非应激大鼠的内脏去神经支配增加了皮质酮脉冲的频率，揭示了肾上腺神经支配的抑制功能。相比之下，手术后一天应激，肾上腺。去神经支配减少肾上腺搏动，提示肾上腺神经支配的刺激功能。为了检验神经对搏动分泌的调节是否由于脏器神经和肾上腺对促肾上腺皮质激素（ACTH）的敏感性的直接作用，用地塞米松治疗的大鼠给予重复的促肾上腺皮质激素脉冲，并测定皮质酮反应的幅度。在手术后2或5天对完整大鼠或对照大鼠(C)和去内脏大鼠（SPLNX）进行检测。术后5天，与SPLNX动物相比，C动物的肾上腺反应性降低。然而，术后2天未见差异。为了确定肾上腺反应性的降低是否涉及细胞或器官水平的机制，分散的肾上腺皮质，从完整或去神经的肾上腺中分离的细胞用ACTH刺激，并测定皮质酮的分泌。与体内实验结果一致，术后5天，而不是1天或2天，去神经支配增加了肾上腺细胞的反应性。这些发现支持神经介导的抑制肾上腺对非应激大鼠ACTH的敏感性。
Awake rats demonstrate an ultradian rhythm in adrenal secretion of corticosterone. Splanchnic denervation in unstressed rats increases the frequency of corticosterone pulses, revealing an inhibitory function of adrenal innervation. In contrast, one day after surgical stress, adrenal. denervation reduces adrenal pulsatility, suggesting a stimulatory function of adrenal innervation. To test whether neural modulation of pulsatile secretion was due to a direct effect of the splanchnic nerve an adrenal sensitivity to adrenocorticotropic hormone (ACTH), rats treated with dexamethasone were administered repetitive pulses of ACTH, and the amplitude of corticosterone responses was determined. Intact or control (C) and splanchnicotomized (SPLNX) rats were tested at 2 or 5 days after surgery. Five days after surgery, adrenal responsiveness in C animals was reduced compared with SPLNX animals. However, no differences were seen 2 days after surgery. To determine whether the reduction in adrenal responsiveness involved a cellular or organ level mechanism, dispersed adrenal cortical, cells isolated from intact or denervated adrenal glands were stimulated with ACTH, and corticosterone secretion was determined. Consistent with in vivo results, denervation increased the responsiveness of adrenal cells obtained 5, but not 1 or 2, days after surgery. These findings support a neurally mediated inhibition of adrenal sensitivity to ACTH in unstressed rats.