The effects of highly selective opioid receptor antagonists on the release of arginine vasotocin induced by hyperosmotic stimulation and angiotensin II injection.

The effects of highly selective antagonists to mu-, delta-, and kappa-opioid receptor subtypes on hyperosmotic- or angiotensin II (AII)-induced arginine vasotocin (AVT) release were investigated in chicks. Plasma levels of AVT increased about 1.5-fold after the administration of 1.5 M NaCl (200 microl, ip) or 100 ng AII (5 microl, icv). The administration of the mu-antagonist naloxonazine and the kappa-antagonist nor-Binaltorphimine further elevated plasma levels of AVT stimulated by hypertonic NaCl or AII. These effects of mu- and kappa-opioid receptor antagonists on AVT release were dose dependent. Nor-Binaltorphimine enhanced hyperosmotically stimulated plasma levels of AVT at a lower dose than that of naloxonazine. Conversely, the delta-selective antagonist naltrindole did not significantly affect AVT secretion. None of the opioid receptor antagonists influenced basal plasma levels of AVT. Therefore, these results suggest that mu- and kappa-opioid receptors are involved in hyperosmotic- and AII-induced AVT release, and the effect of the kappa-opioid receptor antagonist in the AVT release stimulated by hyperosmolality is strong compared to that of the mu-opioid receptor antagonist.