缺乏血管加压素V1A受体的小鼠肾上腺细胞中，精氨酸血管加压素诱导的醛固酮释放受损。
Impaired arginine-vasopressin-induced aldosterone release from adrenal gland cells in mice lacking the vasopressin V1A receptor.
作者信息
Birumachi Jun-ichi, Hiroyama Masami, Fujiwara Yoko, Aoyagi Toshinori, Sanbe Atsushi, Tanoue Akito
机构信息
Department of Pharmacology, National Research Institute for Child Health and Development, 2-10-1 Okura Setagaya-ku, Tokyo 157-8535, Japan.
出版信息
Eur J Pharmacol. 2007 Jul 2;566(1-3):226-30. doi: 10.1016/j.ejphar.2007.03.022. Epub 2007 Mar 24.
We examined aldosterone release in response to stimulation with arginine-vasopressin (AVP) using adrenal gland cells. AVP caused a significant increase in aldosterone release from the dispersed adrenal gland cells of wild-type mice (V1AR+/+) at concentrations from 0.1 microM to 1 microM. In contrast, AVP-induced aldosterone release was impaired in adrenal gland cells from mice lacking the vasopressin V1A receptor (V1AR-/-), while adrenocorticotropic hormone (ACTH)-induced aldosterone release in V1AR-/- mice was not significantly different from that in V1AR+/+ mice. In addition, a vasopressin V1A receptor-selective antagonist 1-[1-[4-(3-acetylaminopropoxy)benzoyl]-4-piperidyl]-3,4-dihydro-2(1H)-quinolinone (OPC-21268) potently inhibited AVP-induced aldosterone release. Thus, our study clearly demonstrates that AVP-induced aldosterone release from adrenal gland cells is mediated via the vasopressin V1A receptor in mice.
我们使用肾上腺细胞研究了精氨酸加压素（AVP）刺激下醛固酮的释放情况。在浓度为0.1微摩尔/升至1微摩尔/升时，AVP可使野生型小鼠（V1AR+/+）分散的肾上腺细胞中醛固酮的释放显著增加。相比之下，缺乏加压素V1A受体（V1AR-/-）的小鼠肾上腺细胞中，AVP诱导的醛固酮释放受损，而促肾上腺皮质激素（ACTH）诱导的V1AR-/-小鼠醛固酮释放与V1AR+/+小鼠相比无显著差异。此外，一种加压素V1A受体选择性拮抗剂1-[1-[4-(3-乙酰氨基丙氧基)苯甲酰基]-4-哌啶基]-3,4-二氢-2(1H)-喹啉酮（OPC-21268）可有效抑制AVP诱导的醛固酮释放。因此，我们的研究清楚地表明，小鼠肾上腺细胞中AVP诱导的醛固酮释放是通过加压素V1A受体介导的。
Zotero 插件