Ono N, Bedran de Castro J, Khorram O, McCann S M
Life Sci. 1985 May 6;36(18):1779-86. doi: 10.1016/0024-3205(85)90561-2.
To determine the role of arginine vasopressin (AVP) in stress-induced release of anterior pituitary hormones, AVP antiserum or normal rabbit serum (NRS) was micro-injected into the 3rd ventricle of freely-moving, ovariectomized (OVX) female rats. A single 3 microliter injection was given, and 24 hours later, the injection was repeated 30 min prior to application of ether stress for 1 min. Although AVP antiserum had no effect on basal plasma ACTH concentrations, the elevation of plasma ACTH induced by ether stress was lowered significantly. Plasma LH tended to increase following ether stress but not significantly so; however, plasma LH following stress was significantly lower in the AVP antiserum-treated group than in the group pre-treated with NRS. Ether stress lowered plasma growth hormone (GH) levels and this lowering was slightly but significantly antagonized by AVP antiserum. Ether stress also elevated plasma prolactin (Prl) levels but these changes were not significantly modified by the antiserum. To evaluate any direct action of AVP on pituitary hormone secretion, the peptide was incubated with dispersed anterior pituitary cells for 2 hours. A dose-related release of ACTH occurred in doses ranging from 10 ng (10 p mole)-10 micrograms/tube, but there was no effect of AVP on release of LH. The release of other anterior pituitary hormones was also not affected except for a significant stimulation of TSH release at a high dose of AVP. The results indicate that AVP is involved in induction of ACTH and LH release during stress. The inhibitory action of the AVP antiserum on ACTH release may be mediated intrahypothalamically by blocking the stimulatory action of AVP on corticotropin-releasing factor (CRF) neurons and/or also in part by direct blockade of the stimulatory action of vasopressin on the pituitary. The effects of vasopressin on LH release are presumably brought about by blockade of a stimulatory action of AVP on the LHRH neuronal terminals.
为了确定精氨酸加压素（AVP）在应激诱导的垂体前叶激素释放中的作用，将AVP抗血清或正常兔血清（NRS）微量注射到自由活动的去卵巢（OVX）雌性大鼠的第三脑室。单次注射3微升，24小时后，在施加1分钟乙醚应激前30分钟重复注射。虽然AVP抗血清对基础血浆促肾上腺皮质激素（ACTH）浓度没有影响，但乙醚应激诱导的血浆ACTH升高显著降低。乙醚应激后血浆促黄体生成素（LH）有升高趋势但不显著；然而，AVP抗血清处理组应激后的血浆LH显著低于NRS预处理组。乙醚应激降低了血浆生长激素（GH）水平，而AVP抗血清对此有轻微但显著的拮抗作用。乙醚应激还升高了血浆催乳素（Prl）水平，但抗血清对这些变化没有显著影响。为了评估AVP对垂体激素分泌的任何直接作用，将该肽与分散的垂体前叶细胞孵育2小时。在剂量范围为10纳克（10皮摩尔）-10微克/管时，促肾上腺皮质激素出现了剂量相关的释放，但AVP对促黄体生成素的释放没有影响。除了在高剂量AVP时对促甲状腺激素（TSH）释放有显著刺激作用外，其他垂体前叶激素的释放也不受影响。结果表明，AVP参与应激期间促肾上腺皮质激素和促黄体生成素释放的诱导。AVP抗血清对促肾上腺皮质激素释放的抑制作用可能通过阻断AVP对促肾上腺皮质激素释放因子（CRF）神经元的刺激作用在下丘脑内介导，和/或部分也通过直接阻断血管加压素对垂体的刺激作用介导。血管加压素对促黄体生成素释放的作用可能是通过阻断AVP对促性腺激素释放激素（LHRH）神经末梢的刺激作用实现的。
