Vasopressin and β-endorphin release after osmotic and non-osmotic stimuli: effect of naloxone and dexamethasone

Abstract

The purpose of this study was to determine whether or not vasopressin release in response to various stimuli in the conscious rat is controlled by endogenous opioid peptides, in particular β-endorphin. Naloxone (1 mg·kg −1 i.m.) promoted vasopressin release in response to both an angiotensin II infusion (500 ng·kg −1·min −1) or an isosmolar, nonhypotensive hypovolaemia achieved by polyethylene glycol injection (PEG, 20% solution i.p.); however, naloxone was without effect when vasopressin release was induced by hypertonic saline injection (2.5% solution i.p.) or a severe fall in arterial blood pressure following trimethidinium (10 mg·kg −1 i.m.) induced ganglionic blockade. Vasopressin release was accompanied by an increase in plasma β-endorphin-like immunoreactivity (β-EI) following an angiotensin II infusion or PEG administration, but not after hypertonic saline or trimethidinium injection. Dexamethasone pretreatment (0.5 mg·kg −1 twice i.p.) prevented the increase in plasma β-EI following an angiotensin II infusion or PEG administration. The simultaneous angiotensin II- or PEG-induced increase in vasopressin release was unaffected or potentiated, respectively, by the glucocorticoid. In contrast, vasopressin release in response to hypertonic saline or trimethidinium injection was significantly inhibited by dexamethasone. We conclude that an inhibitory control by endogenous opiates is involved in some, but not all of the different pathways leading to vasopressin release. The results obtained do not prove but can be reconciled with the proposal that hypophyseal β-endorphin is the compound responsible.