Gonadal steroid modulation of LH secretion stimulated by LHRH, Ca2+ and cAMP.
Primary cultures of enzymatically dispersed rat pituitary cells were used to examine steroid effects on LH secretion stimulated by LHRH, Ca2+ and cAMP. Cultures were pretreated for 48 h with testosterone (T) or 17 beta-estradiol (E) and then challenged for 4 h with various secretogogues. T did not affect basal LH secretion; it inhibited the responses to Ca2+ and LHRH; and it potentiated the response to cAMP. E stimulated both basal LH secretion and the responses to all secretogogues, without affecting cell LH content. Thus, T affects stimulus-secretion coupling, while E affects secretion per se. All steroid effects were blocked by steroid antagonists, indicating that steroid action is receptor-mediated regardless of the secretogogue involved. The similarity of steroid effects on the responses to LHRH and Ca2+ but not cAMP suggests that Ca2+ rather than cAMP is a second messenger for LHRH, and that steroid action occurs at some step subsequent to LHRH-stimulated Ca2+ mobilization.
D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D002452:Cell Count; D002772:Cholera Toxin / Q000494:pharmacology; D000242:Cyclic AMP / Q000494:pharmacology*; D003534:Cyproterone / Q000494:pharmacology; D005260:Female; D012739:Gonadal Steroid Hormones / Q000494:pharmacology*; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology*; D007986:Luteinizing Hormone / Q000378:metabolism*; D009594:Nitromifene / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011956:Receptors, Cell Surface / Q000187:drug effects; D011966:Receptors, LHRH
D012739:Gonadal Steroid Hormones; D011956:Receptors, Cell Surface; D011966:Receptors, LHRH; D007987:Gonadotropin-Releasing Hormone; D000001:Calcimycin; D009594:Nitromifene; D007986:Luteinizing Hormone; D002772:Cholera Toxin; D000242:Cyclic AMP; D003534:Cyproterone; D011188:Potassium; D002118:Calcium