Abstract
A small proportion of brain mineralocorticoid receptors (MR) mediate control of blood pressure, water and electrolyte balance, sodium appetite, and sympathetic drive to the periphery. Circulating inflammatory cytokines modulate MR-mediated changes in sympathoexcitation. Aldosterone binding to MR in the brain occurs, despite concentrations that are 2-3 orders of magnitude less than those of cortisol and corticosterone, which have similar affinity for the MR. The possible mechanisms for selective MR activation by aldosterone, the cellular mechanisms of MR action and the effects of brain MR on hemodynamic homeostasis are considered in this review. MR antagonists are valuable adjuncts to the treatment of chronic cardiovascular and renal disease; the crucial need to discover targets for development of selective therapy for specific MR functions is also discussed.