Jones T H, Brown B L, Dobson P R
Department of Human Metabolism and Clinical Biochemistry, University of Sheffield Medical School.
J Endocrinol. 1988 Mar;116(3):367-71. doi: 10.1677/joe.0.1160367.
Gonadotrophin-releasing hormone (GnRH) stimulated the accumulation of inositol phosphates and prolactin secretion in anterior pituitary cells from young male rats. Saralasin [( Sar1, Ala8]-angiotensin II; a competitive antagonist of angiotensin II) inhibited the increase in both inositol phosphates and prolactin in a dose-dependent manner. Since angiotensin II has been shown to be a potent stimulus for inositol phosphate accumulation and prolactin secretion in the lactotroph, these findings suggest that angiotensin II acts as a paracrine agent, being released from the gonadotroph in response to GnRH and causing the lactotroph to release prolactin through an effect on phosphoinositide metabolism. The ability of GnRH to promote prolactin release was lost in pituitaries from older rats, and the increase in total inositol phosphate accumulation was less. These findings provide evidence of a physiological role for the presence of the renin-angiotensin system within the pituitary gland.
促性腺激素释放激素(GnRH)刺激了幼年雄性大鼠垂体前叶细胞中肌醇磷酸的积累和催乳素的分泌。沙拉新[(Sar1,Ala8)-血管紧张素II;血管紧张素II的竞争性拮抗剂]以剂量依赖的方式抑制了肌醇磷酸和催乳素的增加。由于血管紧张素II已被证明是促乳素细胞中肌醇磷酸积累和催乳素分泌的有效刺激物,这些发现表明血管紧张素II作为一种旁分泌因子,在促性腺激素细胞中响应GnRH释放,并通过对磷酸肌醇代谢的影响导致促乳素细胞释放催乳素。在老年大鼠的垂体中,GnRH促进催乳素释放的能力丧失,总肌醇磷酸积累的增加也较少。这些发现为垂体中肾素-血管紧张素系统存在的生理作用提供了证据。