Aldosterone-induced organ damage: plasma aldosterone level and inappropriate salt status.
Aldosterone-induced organ damage: plasma aldosterone level and inappropriate salt status.
复制标题
醛固酮引起的器官损伤：血浆醛固酮水平和不适当的盐状态。
作者：
A. Sato;T. Saruta
近年来，已有研究表明，醛固酮可通过非上皮性盐皮质激素受体直接损害心脏、血管和肾脏等多种器官，而不依赖于血压的变化。据临床报道，抗醛固酮类药物具有保护器官的作用。近10年来，这些影响一直被认为是重要的，这一事实似乎表明，由于血浆醛固酮水平与盐状态不成比例，可能会导致醛固酮引起的器官损伤。在之前的一项研究中，在低盐饮食下，无法在醛固酮增多症的实验性模型中诱导心脏纤维化。因此，在考虑需要抗醛固酮药物治疗的疾病或状态时，了解血浆醛固酮水平与不适当的盐平衡之间的关系是极其重要的。本文综述了迄今已报道的基础和临床研究，主要探讨了醛固酮和高盐引起器官损害的病理机制。通过血管炎症介导的醛固酮直接器官损伤本质上需要盐，而这与血浆中的醛固酮水平是不合适的，从这一角度进行的研究可能为阐明盐通过非上皮性盐皮质激素受体参与醛固酮的作用提供线索。在人类中，如果盐摄入量与醛固酮水平不平衡，也可能发生器官损伤，即使血浆中的醛固酮水平在正常范围内。这意味着新的醛固酮阻滞剂依普利酮也可能作为一种抑制炎症的药物具有重要意义，可能是器官损伤的触发因素。
In recent years, it has been clarified that aldosterone can directly damage various organs, such as the heart, blood vessel, and kidneys, via non-epithelial mineralocorticoid receptors, independent of changes in blood pressure. Anti-aldosterone drugs have been clinically reported to be useful for their organ-protecting effects. The fact that these effects have been considered important for almost 10 years seems to indicate that aldosterone-induced organ damage can develop as a consequence of plasma aldosterone levels being in disproportion to salt status. In a previous study, cardiac fibrosis could not be induced in an experimental model of hyperaldosteronism with a low-salt diet. It is, therefore, extremely important to understand the relationship between plasma aldosterone level and inappropriate salt balance when considering diseases or states for which an anti-aldosterone drug is called for. In this paper we review the fundamental and clinical studies reported to date, mainly to investigate the pathology of organ damage induced by aldosterone and excess salt. Aldosterone-induced direct organ damage mediated through vasculitis essentially requires salt, which is inappropriate for plasma aldosterone level, and studies performed from this standpoint may provide a clue to the clarification of the involvement of salt in the actions of aldosterone via non-epithelial mineralocorticoid receptors. In humans, it is also strongly suggested that organ damage may occur, even at a plasma aldosterone level within a normal range, if salt intake is imbalanced to the aldosterone level. This means that the new aldosterone blocker eplerenone may also have significance as a drug inhibiting inflammation, possibly serving as a trigger of organ damage.