Tsuzuki S, Matoba T, Eguchi S, Inagami T
Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232-0146, USA.
Hypertension. 1996 Nov;28(5):916-8. doi: 10.1161/01.hyp.28.5.916.
The angiotensin II type 2 (AT2) receptor inhibits basic fibroblast growth factor-induced proliferation of R3T3 fibroblast cells and transiently stimulates a vanadate-sensitive phosphotyrosine phosphatase, strongly suggesting that AT2 is a mitogen inhibitor. We generated AT2 gene-null mice that showed increased blood pressure, indicating the hypotensive action of AT2. However, inhibition of renomedullary AT2 by selective antagonists, as reported by Sassard and associates, show that AT2 suppresses pressure natriuresis. Thus, both AT1 and AT2 work in the direction of sodium retention, suggesting a unique role for angiotensin II in the kidney in terms of blood pressure regulation and sodium metabolism.
血管紧张素II 2型（AT2）受体可抑制碱性成纤维细胞生长因子诱导的R3T3成纤维细胞增殖，并短暂刺激钒酸盐敏感的磷酸酪氨酸磷酸酶，这强烈表明AT2是一种促有丝分裂抑制剂。我们培育出了AT2基因缺失的小鼠，这些小鼠血压升高，表明AT2具有降压作用。然而，正如萨萨德及其同事所报道的，选择性拮抗剂对肾髓质AT2的抑制作用表明，AT2可抑制压力性利钠。因此，AT1和AT2都在钠潴留方面发挥作用，这表明血管紧张素II在肾脏中对血压调节和钠代谢具有独特作用。
