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.