ABSTRACT
The present study was performed to examine the effect of the cyclo-oxygenase inhibitor, indomethacin, and that of various prostaglandins on the release of vasopressin and β-endorphin-like immunoreactivity (β-EI) from the rat neurointermediate lobe of the hypophysis, which was superfused in vitro. Indomethacin (2·8 and 28 μmol/l) changed neither basal secretion of vasopressin nor that evoked by electrical stimulation, whereas the resting release of β-EI was enhanced by indomethacin (28 μmol/l). Prostaglandin (PG) E2 did not influence resting release of vasopressin but markedly inhibited (by about 50%) electrically induced release of vasopressin (least effective concentration: 300 nmol/l) as well as spontaneous secretion of β-EI (least effective concentration: 100 nmol/l) in the presence of indomethacin (28 μmol/l). Prostaglandin F2α (5 μmol/l) also inhibited the evoked release of vasopressin, whereas PGD2 (5 μmol/l) did not. Prostaglandin F2α (5 μmol/l), D2 and I2 (1·5 μmol/l each) produced no effects on β-EI release. As observed in the neurohypophysis, PGE2 inhibited the electrically induced release of vasopressin from the medial basal hypothalamus in vitro. We conclude that prostaglandins (especially PGE2) can inhibit (1) the stimulated release of vasopressin when acting on vasopressin-containing nerve terminals of either neurosecretory system (neurohypophysis, median eminence region), and (2) the secretion of β-EI and, as can be inferred, α-MSH, by a direct action on intermediate lobe cells.
J. Endocr. (1985) 106, 189–195