Aguilera G
Section on Endocrine Physiology, National Institute of Child Health and Human Development, NIH, Bethesda, MD 20892.
Mol Cell Endocrinol. 1992 Dec;90(1):53-60. doi: 10.1016/0303-7207(92)90101-b.
The role of AII receptors subtypes, AT1 and AT2, in the regulation of aldosterone secretion was studied in adrenal glomerulosa cells and membranes from rats on normal and low sodium intake, using AII receptor subtype-specific antagonists. In adrenal glomerulosa cells, more than 90% of the receptors were AT1 and there was a good correlation between the potencies of the antagonists to inhibit ligand binding, and AII-stimulated aldosterone production and inositol phosphate formation. The inhibition of basal and ACTH-stimulated cAMP by AII was also abolished by the AT1, but not the AT2, antagonist. Sodium restriction for 6 days increased both receptor subtypes in the same proportion, but only the AT1 antagonist inhibited AII-stimulated aldosterone production. The data demonstrate that AT1 receptor mediates the regulatory actions of AII in the adrenal zona glomerulosa.
利用血管紧张素II（AII）受体亚型特异性拮抗剂，研究了AII受体亚型AT1和AT2在正常和低钠摄入大鼠肾上腺球状带细胞及细胞膜中对醛固酮分泌调节的作用。在肾上腺球状带细胞中，超过90%的受体为AT1，拮抗剂抑制配体结合的效力、AII刺激的醛固酮生成及肌醇磷酸形成之间存在良好相关性。AT1拮抗剂可消除AII对基础及促肾上腺皮质激素（ACTH）刺激的环磷酸腺苷（cAMP）的抑制作用，而AT2拮抗剂则不能。6天的钠限制使两种受体亚型以相同比例增加，但只有AT1拮抗剂抑制AII刺激的醛固酮生成。数据表明，AT1受体介导了AII在肾上腺球状带的调节作用。
