Meyerhoff J L, Oleshansky M A, Kalogeras K T, Mougey E H, Chrousos G P, Granger L G
Department of Medical Neurosciences, Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.
Adv Exp Med Biol. 1990;274:91-111. doi: 10.1007/978-1-4684-5799-5_6.
We have shown that a psychological stressor can elicit increases in plasma AVP levels in normal human subjects. Since AVP can enhance the release of ACTH, and the pituitary gland is outside the blood-brain barrier, AVP present in the general circulation might extend the time course of stress-induced, CRF-mediated release of ACTH from the anterior lobe. Since PRA is involved in the synthesis of angiotensin I, the precursor of AII, and AII is known to enhance CRF-mediated release of ACTH from pituitary cells and to stimulate release of AVP, it is possible that the increase in PRA also contributed to the release of AVP and ACTH in this study. Reports differ as to whether circulating catecholamines can release ACTH in vivo by direct action on the pituitary. Finally, it has been reported that beta-EP enhances the release of PRL, and inhibits release of AVP. Since the increase in beta-EP in the present study was quite robust, it might have extended the PRL release, and truncated the AVP response.
我们已经表明,心理应激源可使正常人类受试者的血浆抗利尿激素(AVP)水平升高。由于AVP可增强促肾上腺皮质激素(ACTH)的释放,且垂体位于血脑屏障之外,循环中的AVP可能会延长应激诱导的、促肾上腺皮质激素释放因子(CRF)介导的前叶ACTH释放的时间进程。由于肾素活性(PRA)参与血管紧张素I(AII的前体)的合成,且已知AII可增强CRF介导的垂体细胞ACTH释放并刺激AVP释放,因此在本研究中PRA的升高也可能促成了AVP和ACTH的释放。关于循环中的儿茶酚胺是否能通过直接作用于垂体在体内释放ACTH,各报告的结果有所不同。最后,有报道称β-内啡肽(beta-EP)可增强催乳素(PRL)的释放,并抑制AVP的释放。由于本研究中beta-EP的升高相当显著,它可能延长了PRL的释放,并缩短了AVP反应。