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- Jun-ichi Birumachi, Masami Hiroyama, Yoko Fujiwara, Toshinori Aoyagi, Atsushi Sanbe, and Akito Tanoue.
- Department of Pharmacology, National Research Institute for Child Health and Development, 2-10-1 Okura Setagaya-ku, Tokyo 157-8535, Japan.
- Eur. J. Pharmacol. 2007 Jul 2; 566 (1-3): 226-30.
AbstractWe 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.
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