| pubmed-article:6426317 | pubmed:abstractText | Because arachidonic acid and/or its metabolites may be intracellular effectors of calcium-mediated secretion, we studied whether arachidonic acid added exogenously mobilizes calcium and stimulates prolactin secretion from GH3 cells, cloned rat pituitary cells. Arachidonic acid caused efflux of 45Ca from preloaded cells and stimulated prolactin secretion. The concentration dependencies of these effects were similar; stimulation was attained with 3 microM arachidonic acid. To determine indirectly whether these effects may be caused by arachidonic acid itself, not via conversion to metabolites, two experimental approaches were used. First, inhibitors of arachidonic acid metabolism, eicosatetraynoic acid and indomethacin, did not inhibit arachidonic acid-induced prolactin secretion. And second, alpha-linolenic acid, which cannot be converted to arachidonic acid, and linoleic acid, but not saturated fatty acids of equal chain length, stimulated 45Ca efflux and prolactin secretion. These data demonstrate that arachidonic acid added exogenously causes Ca2+ mobilization and prolactin secretion from GH3 cells and suggest that arachidonic acid itself, not via metabolism, may be a cellular regulator of prolactin secretion. | lld:pubmed |
