Effect of LHRH on incorporation of [32P]-orthophosphate into phosphatidylinositol by dispersed anterior pituitary cells.

Stimulated release of luteinizing hormone (LH) from the anterior pituitary in response to luteinizing hormone releasing hormone (LHRH), is apparently controlled by Ca2+-mediated events. In many tissues, when an involvement of Ca2+ in secretion has been found, there is an associated increased metabolic turnover of phosphatidylinositol. The objective of this investigation was to determine the effect of LHRH on the incorporation of [32P]orthophosphate into phosphatidylinositol by anterior pituitary cells maintained in vitro. When anterior pituitary cells were incubated for 5-40 min in the presence of [32P]orthophosphate, phosphatidylinositol and phosphatidylcholine were the most rapidly radiolabelled phospholipids. The addition of LHRH to the cell culture medium at concentrations previously demonstrated to release LH, increased the incorporation of 32P]orthophosphate into phosphatidylinositol in a dose-dependent manner. Incorporation of [32P]orthophosphate into other phospholipids was unaffected by LHRH at all concentrations employed. These results are consistent with the hypothesis that LHRH causes a receptor-mediated increase in turnover of phosphatidylinositol and this may be among the early metabolic events in the mechanism of LHRH-stimulated LH secretion from the anterior pituitary gland.