Leung P C, Raymond V, Labrie F
Endocrinology. 1983 Mar;112(3):1138-40. doi: 10.1210/endo-112-3-1138.
Luteinizing hormone-releasing hormone (LHRH) causes a rapid and marked increase of [32P]orthophosphate incorporation into phosphatidylinositol (PI) and phosphatidic acid (PA) in rat luteal cells in culture. The neurohormone exerts its stimulatory effect at an ED50 value of approximately 15 nM. Human chorionic gonadotropin (hCG) has no effect alone and does not interfere with the LHRH-induced PA-PI labeling. The rapidity and the specificity of the effect of LHRH suggest that the stimulation of the PA-PI cycle may well serve as a potent transducing mechanism responsible for the direct action of LHRH and its agonists at the ovarian level.
促黄体生成激素释放激素（LHRH）可使培养的大鼠黄体细胞中[32P]正磷酸盐掺入磷脂酰肌醇（PI）和磷脂酸（PA）的量迅速且显著增加。该神经激素在约15 nM的半数有效剂量（ED50）值时发挥其刺激作用。人绒毛膜促性腺激素（hCG）单独无作用，且不干扰LHRH诱导的PA-PI标记。LHRH作用的快速性和特异性表明，PA-PI循环的刺激很可能是一种有效的转导机制，负责LHRH及其激动剂在卵巢水平的直接作用。
