Opioid inhibition of secretion from oxytocin and vasopressin nerve terminals following selective depletion of neurohypophysial catecholamines.

Opioids intrinsic to the neurohypophysis inhibit secretion from magnocellular neurosecretory terminals. This study examined whether the actions of opioids are mediated via interactions with neurohypophysial catecholamine systems. Blocking the action of intrinsic opioids in the isolated neurohypophysis with naloxone enhanced evoked secretion of oxytocin (OXT) by 150% and of vasopressin (AVP) by 30%. The enhancement of OXT secretion was not significantly altered in neurohypophyses depleted of greater than 90% of noradrenaline content by prior lesion of the ventral noradrenergic tract, or depleted of greater than 90% of both noradrenaline and dopamine content by prior reserpine treatment. Significant enhancement of AVP secretion by naloxone did not occur following depletion of catecholamines. The data suggest: (1) the majority of the influence of intrinsic opioids on secretion of OXT is not mediated via interaction with noradrenaline or dopamine systems, (2) the weaker influence of intrinsic opioids over AVP secretion may be mediated via catecholamines, (3) the majority of neurohypophysial noradrenaline is derived from projections of ascending medullary cell groups.