Angiotensin stimulates oxytocin release: imparied response in rats with genetic hypothalamic diabetes insipidus.

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.