Abstract
We recently reported that both prostaglandin E2 (PGE2) and arachidonic acid (AA) in the presence of ouabain induced a gradual secretion of catecholamines from cultured bovine adrenal chromaffin cells by stimulation of phosphoinositide metabolism. Because AA is a precursor of PGE2, we examined the relationship between PGE2- and AA-induced catecholamine release from the cells. No inhibitors of cyclooxygenase or lipoxygenase enzymes prevented phosphoinositide metabolism evoked by AA. On the other hand, PGE2 induced rapid hydrolysis of [3H]AA from prelabeled phospholipid pools: the release of [3H]AA could be detected at as early as 15 sec and reached a plateau after 1 min. While phospholipase A2 inhibitors p-bromophenacyl bromide and mepacrine inhibited PGE2-induced AA release, the phospholipase C inhibitor neomycin did not inhibit it. These phospholipase inhibitors blocked PGE2-evoked catecholamine release as well as stimulation of phosphoinositide metabolism. Pretreatment of intact cells with the phorbol ester TPA prevented activation of phospholipase A2 and phospholipase C by PGE2. These results demonstrate that PGE2 induces AA release via direct activation of phospholipase A2 and that the released AA may be involved in PGE2-induced catecholamine release from chromaffin cells.
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