Rivier C, Rivier J, Mormede P, Vale W
Endocrinology. 1984 Sep;115(3):882-6. doi: 10.1210/endo-115-3-882.
Arginine-vasopressin (AVP) acts on vasoconstriction and diuresis through two different types of receptors (V1 and V2, respectively). Since AVP also modifies ACTH release, we have attempted to determine which class of receptors mediates the capacity of AVP to increase ACTH secretion and to potentiate the effect of corticotropin-releasing factor (CRF) on the pituitary using two AVP antagonists: [1-deaminopenicillamine-2-(O-methyl)tyrosine]arginine-vasopressin [dPTyr(Me)-AVP], which blocks V1 receptors, and [1-beta-mercapto-beta,beta-cyclopentamethylene propionic acid)2-D-leucine-4-valine]arginine vasopressin [d(CH2)5DLeuValAVP], which interferes with V2 receptors. dPTyr(Me)AVP, but not d(CH2)5DLeuValAVP, inhibited the ACTH-releasing as well as the CRF-potentiating effects of both AVP and its antidiuretic analog [1-deamino-8-D-arginine]vasopressin (dDAVP). These results suggest that the actions of AVP and dDAVP on the corticotrophs is primarily mediated through V1 (pressor-like) receptors.
精氨酸加压素（AVP）通过两种不同类型的受体（分别为V1和V2）作用于血管收缩和利尿。由于AVP也会改变促肾上腺皮质激素（ACTH）的释放，我们试图使用两种AVP拮抗剂来确定哪一类受体介导AVP增加ACTH分泌以及增强促肾上腺皮质激素释放因子（CRF）对垂体的作用的能力：[1-脱氨青霉胺-2-（O-甲基）酪氨酸]精氨酸加压素[dPTyr（Me）-AVP]，它可阻断V1受体；以及[1-β-巯基-β，β-环亚戊基丙酸）2-D-亮氨酸-4-缬氨酸]精氨酸加压素[d（CH2）5DLeuValAVP]，它会干扰V2受体。dPTyr（Me）AVP而非d（CH2）5DLeuValAVP抑制了AVP及其抗利尿类似物[1-脱氨基-8-D-精氨酸]加压素（dDAVP）的ACTH释放以及CRF增强作用。这些结果表明，AVP和dDAVP对促肾上腺皮质细胞的作用主要是通过V1（类升压）受体介导的。
