Abstract
The aim of this study was to determine whether atrial natriuretic peptide (ANP) alters β-endorphin (β-END) secretion from rat intermediate pituitary and whether this effect is a direct action on the intermediate pituitary or an indirect one mediated by hypothalamic factor (s). We studied the release of β-END from rat neuro-intermediate lobes of the pituitary (NIL) and from the hypothalamo-neurohypophysial complex (HNC), which consists of the hypothalamus, pituitary stalk, intermediate and posterior lobes of the pituitary, by means of an in vitro perifusion system. NIL and HNC were prepared from male Wistar rats and individually perifused for 30 min with perifusion medium followed by 20 min perifusion with medium containing a-rat ANP and/or dopamine (DA). Samples of perifusion medium were collected every 5 min and subjected to RIA for β-END. The basal release of β-END from NIL was 180% of that from HNC (p<0.01), which provides further support for the presence of hypothalamic factors that inhibit β-END release from the intermediate pituitary. The perifusion of HNC with ANP at 10-7 and 10-6M increased the β-END concentration by 25 and 50%, respectively (p<0.01). In contrast, ANP (10-8 to 10-6M) had no effect on β-END release from NIL. The inhibitory eect of DA (10-6M) on β-END release from NIL and HNC (51% and 50% of the basal release, respectively, p<0.01) was confirmed. However, this inhibitory effect was not reversed by ANP: Therefore, it seems unlikely that the stimulatory effect of ANP on β-END release results from antagonizing DA action on the intermediate pituitary.
Since ANP had no direct effect on β-END release from NIL, the stimulatory effect of ANP on the release of β-END is thought to be an indirect one, mediated by hypothalamic factor (s).
