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Selective antagonism of the AT1 receptor inhibits angiotensin II stimulated DNA and protein synthesis in primary cultures of human proximal tubular cells

机译:AT1受体的选择性拮抗作用抑制人类近端肾小管细胞原代培养物中血管紧张素II刺激的DNA和蛋白质合成

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Selective antagonism of the AT1 receptor inhibits angiotensin II stimulated DNA and protein synthesis in primary cultures of human proximal tubular cells. The hypertrophy of renal proximal tubular cells occurs as an adaptive response to a variety of stimuli and may be involved with the progression of renal disease. Angiotensin II acting alone or in combination with other growth factors has been implicated in this process. The aims of this study were to identify the role of both angiotensin II and the angiotensin receptor subtypes in DNA synthesis and protein synthesis in human renal proximal tubular cells. Primary cultures of human renal M, proximal tubular cells were incubated with angiotensin II (10-10 M, 10-8 M, 10-10 M) for 24 to 120 hours either alone or in combination with losartan, PD123319 or 8-bromo-cAMP. Incubation of human proximal tubular cells with angiotensin II (10-10 M, 10-8 M) induced a significant early increase in [3H]thymidine uptake by 19% and 56% (P 1 receptor and dependent upon the inhibition of adenylate cyclase.
机译:在人近端肾小管细胞的原代培养物中,AT1受体的选择性拮抗作用抑制了血管紧张素II刺激的DNA和蛋白质的合成。肾近端肾小管细胞肥大是对多种刺激的适应性反应,可能与肾脏疾病的进展有关。单独或与其他生长因子联合作用的血管紧张素II已牵涉该过程。这项研究的目的是确定血管紧张素II和血管紧张素受体亚型在人肾近端肾小管细胞的DNA合成和蛋白质合成中的作用。将人肾M,近端肾小管细胞的原代培养物与血管紧张素II(10-10 M,10-8 M,10-10 M)单独或与氯沙坦,PD123319或8-溴-营。将人类近端肾小管细胞与血管紧张素II(10-10 M,10-8 M)一起孵育可导致[3H]胸苷的早期摄取显着增加,增加19%和56%(P 1受体,取决于对腺苷酸的抑制作用)环化酶。

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