Possible mechanisms responsible for mineralocorticoid-induced renal injury

越来越多的证据表明，除了血管紧张素II外，醛固酮还参与高血压和肾脏疾病的发病机制。 我们已经证明，醛固酮引起肾损伤，通过激活MR在醛固酮输注大鼠，达尔盐敏感性高血压大鼠，但在血管紧张素II输注高血压小鼠。 在肾脏中，MR不仅在终末小管中表达，而且在肾小球系膜细胞、足细胞、近端小管细胞和成纤维细胞中表达。在这些细胞中，MR激活通过氧化应激和衰老引起细胞损伤。 这些数据表明，MR阻滞剂为高血压和肾损害患者提供了一种潜在的治疗方法。

There is increasing evidence implicating aldosterone, in addition to angiotensin II, in the pathogenesis of hypertension and renal diseases. We have demonstrated that aldosterone causes renal injury through the activation of MR in aldosterone-infused rats, Dahl salt-sensitive hypertensive rats, but in angiotensin II-infused hypertensive mice. In the kidney, MR is expressed not only in destal tubules, but also in glomerular mesangial cells, podocytes, proximal tubular cells, and fibroblasts. In these cells, MR activation causes cell injury via oxidative stress and senescence. These data suggest that MR blockers provide a potential therapeutic approach for patients with hypertension and renal impairment.