The actions of opioids on electrically evoked release of oxytocin, vasopressin, and noradrenaline – using the [<sup>3</sup>H]-noradrenaline technique – from the rat neurohypophysis were examined in vitro. Antagonism of the action of endogenous neurohypophysial opioids with naloxone enhanced release of peptides and [<sup>3</sup>H]-noradrenaline differentially. Naloxone enhanced oxytocin release by 100 and 173% in two series of experiments (ED50 7× 10<sup>–7</sup> M), whilst vasopressin release was enhanced by only 30 and 20%, respectively. [<sup>3</sup>H]-noradrenaline release was maximally enhanced by 41% (ED50 2× 10<sup>–7</sup> M). We examined the opioid receptor subtypes mediating these effects using selective receptor agonists. The ĸ-agonist U-50,488H inhibited oxytocin and vasopressin release to a similar extent, but did not modify [<sup>3</sup>H]-noradrenaline release. The effects of U-50,488H were completely prevented by a tenfold molar excess of naloxone. The µ-agonist (Z)-Ala<sup>2</sup>, MePhe<sup>5</sup> Gly-ol)-enkephalin also failed to inhibit [<sup>3</sup>H]-noradrenaline release and caused only a minor inhibition of oxytocin and vasopressin secretion. The δ-agonist (D-Pen<sup>2</sup>, D-Pen<sup>5</sup>)-enkephalin was without effect. We conclude that (1) ĸ-re-ceptors sensitive to U-50,488H mediate opioid inhibition of secretion from oxytocin and vasopressin nerve terminals; (2) when opioid actions are blocked by naloxone, opioid peptides within the neurohypophysis are shown to exert a much greater influence over oxytocin compared to vasopressin terminals; (3) neurohypophysial opioids also regulate release from noradrenergic terminals, although the nature of the receptors involved remains unclear, and (4) ĸ-receptors can mediate inhibition of neurohormone secretion by an action independent of the neurohypophysial noradrenergic innervation.