title: Protective effect of dietary potassium against cardiovascular damage in salt-sensitive hypertension: possible role of its antioxidant action.
abstract: It is well known that high salt intake induces hypertension and cardiovascular damage, while dietary potassium supplementation counteracts these harmful effects. Actually, the protective effect of potassium is strengthened with excess salt as compared with salt depletion. Although the precise mechanisms have not been fully elucidated, in our previous reports, the antihypertensive effect of dietary potassium was accompanied by sympathetic nerve inhibition in salt-sensitive hypertension. Also, potassium supplement suppressed salt-induced insulin resistance. These effects of dietary potassium can explain its cardio- and vasculo-protective action in addition to the potassium supplementation induced decreased salt-induced rise in blood pressure. On the other hand, salt-sensitive hypertension is associated with reactive oxygen species (ROS) overproduction. Moreover, sympathoexcitation can be induced by central ROS upregulation and insulin resistance can be caused by ROS excess in the target organs of insulin, such as skeletal muscle. Conversely, the seemingly different actions of potassium can be explained by the antioxidant effect of dietary potassium; in our recent studies, potassium supplementation inhibits salt-induced progress of cardiac diastolic dysfunction and vascular neointima formation by cuff placement around arteries, associated with the inhibition of regional ROS overproduction, in salt-sensitive hypertension. Thus, it is possible that dietary potassium protects against salt-induced cardiovascular damage by the reduction of ROS generation and by central sympatholytic action and amelioration of insulin resistance induced through its antioxidant effect.
authors.affiliation: Department of Nephrology and Endocrinology, University of Tokyo Graduate School of Medicine, Tokyo, 112-8655, Japan. katsua-tky@umin.ac.jp
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Ando
authors.forename: Hiromitsu
authors.initials: H
authors.lastname: Matsui
authors.forename: Megumi
authors.initials: M
authors.lastname: Fujita
authors.forename: Toshiro
authors.initials: T
authors.lastname: Fujita
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002318:Cardiovascular Diseases / Q000150:complications / Q000503:physiopathology* / Q000517:prevention & control*; D019587:Dietary Supplements; D018450:Disease Progression; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy*; D007333:Insulin Resistance / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology; D017419:Potassium, Dietary / Q000627:therapeutic use*; D017382:Reactive Oxygen Species / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage / Q000009:adverse effects*; D012982:Sodium, Dietary / Q000008:administration & dosage / Q000009:adverse effects; D013564:Sympathetic Nervous System / Q000503:physiopathology
chemical_list: D000975:Antioxidants; D017419:Potassium, Dietary; D017382:Reactive Oxygen Species; D017673:Sodium Chloride, Dietary; D012982:Sodium, Dietary