Anterior pituitary quarters were incubated in vitro and the release of β-endorphin-like (β-End-IR) and adrenocorticotropin-like immunoreactivity (ACTH-IR) was determined. The effect of phospholipase A2 as well as the effect of various compounds known to influence arachidonic acid metabolism under certain conditions were examined. Phospholipase A2 increased the release of β-End-IR and ACTH-IR. This effect was reversible, concentration-dependent (1–400 ng/ml) and inhibited in calcium-free medium and in the presence of CoCl2 (5 mM) or phospholipase A2 inhibitors (p-bromophenacylbromide, 21 µM; mepacrine, 1 mM). The phospholipase A2-induced β-End-IR release was accompanied by the release of prostaglandin E2. Inhibition of cyclooxygenase activity by indomethacin (14 or 140 µM) did not change β-End-IR release induced by phospholipase A2 (5 ng/ml). The effects of blockers of lipoxygenase (nordihydroguaiaretic acid, NDGA; AA861) or lipoxygenase plus cyclooxygenase (BW755C; eicosatetraynoic acid, ETYA) on phospholipase A2-induced release of β-End-IR were diverse. BW755C (up to 250 µM) and AA861 (up to 100 µM) produced no effect. However, NDGA or ETYA inhibited phospholipase A2-induced β-End-IR release. NDGA (100 µM) produced a maximum inhibition by about 40% (p < 0.05), whereas ETYA (100 µM) produced a maximum inhibition by about 85% (p < 0.001). These data are consistent with the view that phospholipase A2 releases endogenous arachidonic acid which is transformed into products which stimulate ACTH and β-endorphin release from the corticotrophs; the metabolizing enzyme (possibly a lipoxygenase or epoxygenase) is sensitive to NDGA and especially to ETYA.

Keywords:
β-Endorphin release, ACTH release, Anterior pituitary, Phospholipase A2, Cyclooxygenase, Lipoxygenase, Arachidonic acid metabolites
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© 1986 S. Karger AG, Basel
1986
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