17-Beta-Estradiol Potentiates Luteinizing Hormone Glycosylation and Release Induced by Veratridine, Diacylglycerol, and Phospholipase C in Rat Anterior Pituitary Cells

We determined the effect of 17 beta-estradiol (E2) on synthesis and release of luteinizing hormone (LH) induced by drugs which activate intracellular signal transduction mechanisms in rat anterior pituitary cells. Cells were pretreated with E2 (6 x 10(-10) M) or diluent for 24 h, then washed and incubated for 4 h with E2 or diluent, respectively, in the presence or absence of drugs. LH translation and glycosylation were monitored by measuring incorporation of [14C]alanine and [3H]glucosamine, respectively, into total (medium plus cells) immunoprecipitable LH. Immunoreactive LH (IRLH) was measured by radioimmunoassay. Gonadotropin-releasing hormone (GnRH, 1 nM), veratridine (5 microM), L-alpha-1,2-dioctanoyl glycerol (C8, 200 microM), and phospholipase C (PLC, 0.24 U/ml) all increased (p less than 0.01) medium IRLH, [3H]glucosamine-LH, and [14C]alanine-LH, and total [3H]glucosamine-LH in both E2- and diluent-treated cells. Total IRLH or [14C]alanine-LH were not increased by any treatment. E2 alone slightly increased (p less than 0.05) basal medium IRLH and [3H]glucosamine-LH. The stimulatory effects of E2 on basal medium [14C]alanine-LH and total [3H]glucosamine-LH were inconsistent. E2 potentiated (p less than 0.01) the effects of veratridine, C8, PLC, and GnRH on medium IRLH, and medium and total [3H]glucosamine-LH. E2 also potentiated (p less than 0.01) the effects of veratridine, PLC, and GnRH, but not of C8, on medium [14C]alanine-LH. In contrast, E2 did not increase either precursor uptake or incorporation of precursor into total protein in the presence of any secretagogue.(ABSTRACT TRUNCATED AT 250 WORDS)