Rainey W E, Bird I M, Mason J I, Carr B R
Cecil H. and Ida Green Center for Reproductive Biology Sciences, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas 75235-9032.
Am J Obstet Gynecol. 1992 Dec;167(6):1679-85. doi: 10.1016/0002-9378(92)91761-x.
Our objective was to determine if angiotensin II receptors are present on adrenal cells isolated from the human fetal zone and neocortex and to investigate if angiotensin II affects steroid production by these cells.
Primary cultures of both fetal zone and neocortex cells were prepared from fetal adrenal glands. Experiments were conducted to examine the binding of radiolabeled angiotensin II, angiotensin II activation of phospholipase C, and angiotensin II effects on steroidogenesis.
The majority of angiotensin II binding sites were of the type 1 subtype, as determined by displacement of radiolabeled angiotensin with specific receptor antagonists. Angiotensin II caused an increase in tritiated inositol phosphate accumulation in both neocortex and fetal zone cells. This increase could be blocked by type 1 angiotensin II receptor antagonists. Angiotensin II stimulated the production of cortisol, dehydroepiandrosterone, and dehydroepiandrosterone sulfate production during treatment for 2 days. The stimulation by angiotensin II, however, was substantially less than that seen in response to corticotropin treatment.
The human fetal adrenal gland contains type 1 angiotensin II receptors early in gestation. The number of these receptors, albeit low, is sufficient to activate inositol phosphate production and steroidogenesis.
我们的目的是确定从人胎儿带和新皮质分离的肾上腺细胞上是否存在血管紧张素II受体，并研究血管紧张素II是否影响这些细胞的类固醇生成。
从胎儿肾上腺制备胎儿带和新皮质细胞的原代培养物。进行实验以检测放射性标记的血管紧张素II的结合、血管紧张素II对磷脂酶C的激活以及血管紧张素II对类固醇生成的影响。
通过用特异性受体拮抗剂置换放射性标记的血管紧张素确定，大多数血管紧张素II结合位点为1型亚型。血管紧张素II导致新皮质和胎儿带细胞中氚化肌醇磷酸积累增加。这种增加可被1型血管紧张素II受体拮抗剂阻断。在处理2天时，血管紧张素II刺激了皮质醇、脱氢表雄酮和硫酸脱氢表雄酮的产生。然而，血管紧张素II的刺激作用明显小于促肾上腺皮质激素处理后的作用。
人胎儿肾上腺在妊娠早期含有1型血管紧张素II受体。这些受体的数量虽然少，但足以激活肌醇磷酸的产生和类固醇生成。
