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首页> 美国卫生研究院文献>Endocrinology >Subdiaphragmatic Vagotomy Prevents Drinking-Induced Reduction in Plasma Corticosterone in Water-Restricted Rats
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Subdiaphragmatic Vagotomy Prevents Drinking-Induced Reduction in Plasma Corticosterone in Water-Restricted Rats

机译：dia下迷走神经切断术可预防水禁大鼠血浆皮质酮的饮酒诱导减少

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Dehydrated rats exhibit a rapid inhibition of the hypothalamic-pituitary-adrenal axis after rehydration. Drinking activates vagal afferents that project to neurons in the nucleus tractus solitarius (NTS). We hypothesized that when dehydrated rats drink, vagal afferents stimulate NTS neurons initiating inhibition of hypothalamic-pituitary-adrenal activity. Experiments assessed NTS activity by measuring Fos expression. Rats were water restricted for 1 or 6 d, limiting access to water to 30 min/d in the morning. Drinking after single or repeated restriction increased Fos, demonstrating increased NTS activity. We next examined the contribution of the vagus by comparing hormonal responses after total subdiaphragmatic vagotomy or sham surgery. Water restriction for 6 d increased plasma arginine vasopressin (AVP), ACTH, and adrenal and plasma corticosterone in both groups. In sham rats, drinking reduced plasma AVP, ACTH, adrenal and plasma corticosterone by 7.5 min. In total subdiaphragmatic vagotomy rats, whereas drinking reduced plasma AVP, ACTH, and adrenal corticosterone, drinking did not reduce plasma corticosterone. To identify the source of vagal activity, hormonal responses to restriction-induced drinking were measured after common hepatic branch vagotomy (HBV). Although pituitary hormonal responses were not affected by HBV, the adrenal and plasma corticosterone responses to water restriction were reduced; in addition, drinking in HBV rats decreased adrenal corticosterone without changing plasma corticosterone. These data indicate that an intact vagus is necessary to reduce plasma corticosterone when water-restricted rats drink and that the common hepatic vagal branch contributes to the response. These findings implicate the vagus in augmenting rapid removal of circulating corticosterone during relief from stress.
机译：补液后，脱水大鼠表现出对下丘脑-垂体-肾上腺轴的快速抑制。饮酒会激活迷走神经，这些迷走神经会投射到孤束核（NTS）中的神经元。我们假设脱水大鼠喝酒后，迷走神经传入刺激NTS神经元，从而开始抑制下丘脑-垂体-肾上腺的活动。实验通过测量Fos表达来评估NTS活性。将大鼠禁水1或6天，以限制每天早上喝水30分钟。单次或重复限制后喝酒会增加Fos，表明NTS活性增加。接下来，我们通过比较全dia下迷走神经迷走神经切断术或假手术后的激素反应来检查迷走神经的作用。两组的限水时间均增加了6天，血浆精氨酸加压素（AVP），ACTH以及肾上腺和血浆皮质酮水平升高。在假大鼠中，饮酒可使血浆AVP，ACTH，肾上腺和血浆皮质酮降低7.5分钟。在全部dia下迷走神经迷走神经切断大鼠中，饮酒会降低血浆AVP，ACTH和肾上腺皮质激素，而饮酒并不能降低血浆皮质酮。为了确定迷走神经活动的来源，在普通肝分支迷走神经切断术（HBV）后，测量了对限制诱导饮酒的激素反应。尽管垂体激素反应不受HBV的影响，但肾上腺和血浆皮质酮对水分限制的反应有所降低；此外，在HBV大鼠中饮酒可降低肾上腺皮质激素水平，而不会改变血浆皮质激素水平。这些数据表明，缺水大鼠喝水时，完整的迷走神经对于减少血浆皮质酮是必要的，而共同的肝迷走神经分支也有助于这种反应。这些发现暗示迷走神经在减轻压力的过程中增强了循环皮质酮的快速清除。

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