Effect of subdiaphragmatic vagotomy and cholinergic agents in the hypothalamic-pituitary-adrenal axis activity.
Effect of subdiaphragmatic vagotomy and cholinergic agents in the hypothalamic-pituitary-adrenal axis activity.
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膈下迷走神经切断术和胆碱能药物对下丘脑-垂体-肾上腺轴活动的影响。
DOI：
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发表时间：
2007
影响因子：
2.2
通讯作者：
A. Gądek
中科院分区：
文献类型：
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作者：
A. Bugajski;D. Zurowski;P. Thor;A. Gądek
在本研究中，我们研究了迷走神经是否参与介导胆碱能毒蕈碱和烟碱激动剂卡巴胆碱和尼古丁对下丘脑-垂体-肾上腺（HPA）轴的刺激。使用外周（i. p.）和脑室内（i. c. v.）施用卡巴胆碱、硫酸阿托品（AtrS）和氢溴酸阿托品（AtrBr）。腹腔注射氨甲酰胆碱（0.5 mg/kg）诱导的皮质酮反应被腹腔注射AtrBr（0.1 mg/kg）预处理显著降低，但没有被i. c. v. AtrS（0.1 mug）降低。i. c. v.卡巴胆碱（2 μ g）诱导的皮质酮分泌增加被i. c. v. AtrS（0.1 μ g）预处理完全消除，但i. p. AtrBr未改变。与假手术大鼠的反应相比，2周前进行的蛛网膜下迷走神经切断术显著降低了腹腔注射卡巴胆碱（0.2 mg/kg）诱导的ACTH反应，并显著增强了ACTH和皮质酮对较高剂量卡巴胆碱（0.5 mg/kg）的反应。迷走神经切断术消除了低剂量（1 mg/kg）i. p.尼古丁对ACTH和皮质酮分泌的刺激作用;对较高剂量（2.5 mg/kg）的ACTH反应显著降低，而皮质酮反应不受影响。这些结果表明，静脉注射卡巴胆碱通过刺激中枢胆碱能毒蕈碱受体引起相当大的皮质酮反应。卡巴胆碱诱导的皮质酮分泌的主要部分来自外周胆碱能毒蕈碱受体刺激。蛛网膜下迷走神经切断术适度增强了卡巴胆碱诱导的ACTH和皮质酮分泌。迷走神经切断术显著减少尼古丁诱导的ACTH分泌，可能是迷走神经传入的参与。尼古丁诱导的皮质酮分泌并不完全受循环ACTH的调节，而是受各种肾上腺内调节成分的调节。
In the present study, we examined whether the vagus nerve is involved in mediating the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by cholinergic muscarinic and nicotinic agonists, carbachol and nicotine. The site of HPA axis muscarinic stimulation was determined using peripheral (i.p.) and intracerebroventricular (i.c.v.) administration of carbachol, atropine sulphate (AtrS) and atropine hydrobromide (AtrBr). The i.p. carbachol-(0.5 mg/kg)-induced corticosterone response was significantly reduced by i.p. pretreatment with AtrBr (0.1 mg/kg), but was not diminished by i.c.v. AtrS (0.1 mug). The increase in corticosterone secretion induced by i.c.v. carbachol (2 microg) was totally abolished by i.c.v. pretreatment with AtrS (0.1 microg) but was not altered by i.p. AtrBr. Subdiaphragmatic vagotomy performed 2 weeks earlier substantially decreased the i.p. carbachol (0.2 mg/kg)-induced ACTH response and markedly augmented ACTH and corticosterone response to a higher dose of carbachol (0.5 mg/kg) in comparison with the responses in sham operated rats. Vagotomy abolished the stimulatory effect of i.p. nicotine in a low dose (1 mg/kg) on ACTH and corticosterone secretion; the ACTH response to higher dose (2.5 mg/kg) was considerably reduced, while corticosterone response remained unaffected. These results suggest that carbachol given i.c.v. evokes considerable corticosterone response by stimulation of central cholinergic muscarinic receptors. A major part of the i.p. carbachol-induced corticosterone secretion results from peripheral cholinergic muscarinic receptor stimulation. Subdiaphragmatic vagotomy moderately intensified the carbachol-induced ACTH and corticosterone secretion. Vagotomy significantly reduced the nicotine-induced ACTH secretion, possibly by the involvement of vagal afferents. The nicotine-induced corticosterone secretion is not exclusively regulated by circulating ACTH but by various intra-adrenal regulatory components.