Differential effects of various opioid peptides on vasopressin and oxytocin release from the rat pituitary in vitro

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Abstract
Dynorphin (1–17), and to a lesser extent, β-endorphin and [Leu]enkephalin (10−6 M each) decreased the spontaneous release of vasopressin (VP) from the rat neurointermediate pituitary in vitro, whereas the oxytocin (OT) release remained unchanged. Naloxone, however, did not significantly alter the spontaneous VP and OT release. Dynorphin (1–17) (10−7 M) increased the electrically evoked release of VP and OT, while 10−6 M had a significant, somewhat less pronounced stimulatory effect only on VP, but not on OT release. The opiate inactive fragment [des-Tyr1]dynorphin (1–17) did not change the evoked VP and OT release, indicating that the dynorphin effect was mediated by opiate receptors. β-Endorphin (10−6 M and 10−7 M) did not alter the evoked VP and OT secretion. 10−6 M [Leu]enkephalin induced a stimulation of the evoked OT, but not VP release; 10−7 M [Leu]enkephalin had no effect, neither on VP nor on OT release. The opiate antagonist naloxone 10−5 M) induced an increase in the evoked VP and, even more pronounced, OT release. In a concentration of 10−6 M, however, naloxone only increased the evoked OT release. When naloxone and dynorphin (1–17) were concomitantly applied, their stimulatory effects on the evoked VP and OT release were additive. Similarly to the effects of naloxone, addition of a monoclonal antibody which binds to the common N-terminal sequence of all endogenous opioid peptides, resulted in a marked increase in the evoked secretion of VP and, to an even more pronounced degree, of OT. Thus, the stimulated VP and OT release seems to be under a tonic inhibitory control of opioids. Electrical stimulation was found to enhance the release of endogenous immunoreactive dynorphin from the neurointermediate pituitary, while the release of immunoreactive β-endorphin was even decreased. In conclusion, the present data indicate a dual role of endogenous opioid peptides in the VP and OT secretion at the level of the posterior pituitary.