Effect of prostaglandin E2 on ACTH and β-endorphin release from rat adenohypophysis in vitro after secretagogues which can mimic various first or second messengers
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Concentration-response curves of the effect of vasopressin on the release of β-endorphin-like (β-End-IR) and ACTH-like immunoreactivity (ACTH-IR) were constructed in the absence or presence of a fixed concentration of PGE2. The concentration-response curve of vasopressin was shifted to the right about 8-fold by PGE2 (1 μmol/l) without altering the maximum effect.
PGE2 (60 nmol/l–1 μmol/l) markedly reduced β-End-IR release induced by 8-bromoadenosine-3′,5′-cyclicmonophosphate (8Br-cAMP) (1 mmol/l). Omission of Ca2+ from the incubation medium did not prevent PGE2-induced inhibition of 8Br-cAMP-evoked secretion.
4β-Phorbol, 12β-myristate, 13α-acetate (PMA) stimulated β-End-IR and ACTH-IR release in a concentration-dependent manner. This effect was not blocked by indometacin or eicosatetraynoic acid. PG E2 (>100 nmol/l) reduced PMA (100 nmol/l)-elicited secretion by about 50%.
PG E2 (1 μmol/l) almost halved β-End-IR release caused by K+ (30 mmol/l).
After pre-incubation in Ca2+-free medium, re-introduction of Ca2+ (1.3 mmol/l) elicited β-End-IR release. This response was abolished by PG E2 (1 μmol/l).
The addition of Ba2+ (10 mmol/l) to a Ca2+-free medium markedly enhanced β-End-IR release. The stimulation by Ba2+ was blocked by elevating the Ca2+ concentration to 15.3 mmol/l. PGE2 (1 μmol/l) did not influence the Ba2+-induced secretion.
These data suggest that PGE2 inhibits receptor-mediated stimulation of β-End-IR/ACTH-IR release in an apparently competitive manner. We conclude that the ability of PGE2 to inhibit secretion from corticotrophs is not linked to a particular post-receptor mechanism but depends on the interference with a mechanism which follows second messenger formation and which, furthermore, is crucial for exocytotic release mechanisms, e.g. the intracellular availability of calcium.
Key wordsβ-Endorphin release Adrenocorticotropin release Prostaglandin E2 action Phorbol ester Barium
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