Lang R E, Rascher W, Heil J, Unger T, Ganten D
Eur J Pharmacol. 1982 Sep 10;83(1-2):113-7. doi: 10.1016/0014-2999(82)90293-x.
Intracerebroventricularly (i.c.v.) administered angiotensin II (ANG II) at a dose of 100 ng caused a large increase in plasma oxytocin levels in Long Evans (LE) rats and in rats heterozygous for hypothalamic diabetes insipidus (HZ). In rats homozygous for diabetes insipidus (DI) even 100 fold higher doses of ANG II i.c.v. exerted only marginal effects on oxytocin release. The impaired responsiveness in DI rats was fully restored by prolonged treatment with a vasopressin (AVP) analogue. These data show that the decreased sensitivity of ANG II receptors in DI rats is due to the AVP defect and its metabolic consequences and can be reversed by AVP substitution.
向长 Evans（LE）大鼠和下丘脑性尿崩症杂合子（HZ）大鼠脑室内（i.c.v.）注射剂量为 100 ng 的血管紧张素 II（ANG II），可使血浆催产素水平大幅升高。在尿崩症纯合子（DI）大鼠中，即使脑室内注射剂量高出 100 倍的 ANG II，对催产素释放也仅产生轻微影响。通过使用血管加压素（AVP）类似物进行长期治疗，DI 大鼠受损的反应性得以完全恢复。这些数据表明，DI 大鼠中 ANG II 受体敏感性降低是由于 AVP 缺陷及其代谢后果所致，并且可以通过 AVP 替代来逆转。
