title: The kidneys and aldosterone/mineralocorticoid receptor system in salt-sensitive hypertension.
abstract: Strong evidence supports the ability of the aldosterone/mineralocorticoid receptor (MR) system to dominate long-term blood pressure control. It is also increasingly recognized as an important mediator of cardiovascular and renal diseases, particularly in the presence of excessive salt intake. In a subgroup of individuals with metabolic syndrome, adipocyte-derived aldosterone-releasing factors cause inappropriate secretion of aldosterone in the adrenal glands during salt loading, resulting in the development of salt-induced hypertension and cardiac and renal damage. On the other hand, emerging data reveal that aldosterone is not a sole regulator of MR activity. We have identified the signaling crosstalk between MR and small GTPase Rac1 as a novel pathway to facilitate MR signaling. Such a local control system for MR can also be relevant to the pathogenesis of salt-sensitive hypertension, and future studies will clarify the detailed mechanism for the intricate regulation of the aldosterone/MR cascade.
authors.affiliation: Department of Nephrology and Endocrinology, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan. ssiba-tky@umin.ac.jp
authors.forename: Shigeru
authors.initials: S
authors.lastname: Shibata
authors.forename: Toshiro
authors.initials: T
authors.lastname: Fujita
mesh_terms: D000450:Aldosterone / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D018161:Receptors, Mineralocorticoid; D015398:Signal Transduction; D017673:Sodium Chloride, Dietary / Q000009:adverse effects
chemical_list: D018161:Receptors, Mineralocorticoid; D017673:Sodium Chloride, Dietary; D000450:Aldosterone