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  • Title: Inhibition by prostaglandin E2 of the release of vasopressin and beta-endorphin from rat pituitary neurointermediate lobe or medial basal hypothalamus in vitro.
    Author: Knepel W, Nutto D, Vlaskovska M, Kittel C.
    Journal: J Endocrinol; 1985 Aug; 106(2):189-95. PubMed ID: 3160802.
    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 beta-endorphin-like immunoreactivity (beta-EI) from the rat neurointermediate lobe of the hypophysis, which was superfused in vitro. Indomethacin (2.8 and 28 mumol/l) changed neither basal secretion of vasopressin nor that evoked by electrical stimulation, whereas the resting release of beta-EI was enhanced by indomethacin (28 mumol/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 beta-EI (least effective concentration: 100 nmol/l) in the presence of indomethacin (28 mumol/l). Prostaglandin F2 alpha (5 mumol/l) also inhibited the evoked release of vasopressin, whereas PGD2 (5 mumol/l) did not. Prostaglandin F2 alpha (5 mumol/l), D2 and I2 (1.5 mumol/l each) produced no effects on beta-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 beta-EI and, as can be inferred, alpha-MSH, by a direct action on intermediate lobe cells.
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