title: Protective effect of potassium against the hypertensive cardiac dysfunction: association with reactive oxygen species reduction.
abstract: Potassium supplementation has a potent protective effect against cardiovascular disease, but the precise mechanism of it against left ventricular abnormal relaxation, relatively early functional cardiac alteration in hypertensive subjects, has not been fully elucidated. In the present study, we investigated the effect of potassium against salt-induced cardiac dysfunction and the involved mechanism. Seven- to 8-week-old Dahl salt sensitive rats were fed normal diet (0.3% NaCl) or high-salt diet (8% NaCl) with or without high potassium (8% KCl) for 8 weeks. Left ventricular relaxation was evaluated by the deceleration time of early diastolic filling obtained from Doppler transmitral inflow, the slope of the pressure curve, and the time constant at the isovolumic relaxation phase. High-salt loading induced a significant elevation of blood pressure and impaired left ventricular relaxation, accompanied by augmentation of reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activity in the cardiac tissue, measured by the lucigenin chemiluminescence method. Blood pressure lowering by hydralazine could not ameliorate NADPH oxidase activity and resulted in no improvement of left ventricular relaxation. Interestingly, although the blood pressure remained high, potassium supplementation as well as treatment with 4-hydroxy-2,2,6,6-tetramethyl-piperidine-N-oxyl, a superoxide dismutase mimetic, not only reduced the elevated NADPH oxidase activity but also improved the left ventricular relaxation. In conclusion, a high-potassium diet has a potent protective effect on left ventricular active relaxation independent of blood pressure, partly through the inhibition of cardiac NADPH oxidase activity. Sufficient potassium supplementation might be an attractive strategy for cardiac protection, especially in the salt-sensitive hypertensive subjects.
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
authors.forename: Hiromitsu
authors.initials: H
authors.lastname: Matsui
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Shimosawa
authors.forename: Yuzaburo
authors.initials: Y
authors.lastname: Uetake
authors.forename: Hong
authors.initials: H
authors.lastname: Wang
authors.forename: Sayoko
authors.initials: S
authors.lastname: Ogura
authors.forename: Tomoyo
authors.initials: T
authors.lastname: Kaneko
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Ando
authors.forename: Toshiro
authors.initials: T
authors.lastname: Fujita
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D019587:Dietary Supplements; D004195:Disease Models, Animal; D004452:Echocardiography; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006973:Hypertension / Q000150:complications / Q000178:diet therapy / Q000503:physiopathology*; D008297:Male; D019255:NADPH Oxidases / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D011189:Potassium Chloride / Q000008:administration & dosage; D017419:Potassium, Dietary / Q000627:therapeutic use*; D051381:Rats; D020303:Rats, Inbred Dahl; D017382:Reactive Oxygen Species / Q000378:metabolism*; D017673:Sodium Chloride, Dietary; D018487:Ventricular Dysfunction, Left / Q000150:complications / Q000503:physiopathology* / Q000517:prevention & control*
chemical_list: D017419:Potassium, Dietary; D017382:Reactive Oxygen Species; D017673:Sodium Chloride, Dietary; D011189:Potassium Chloride; D019255:NADPH Oxidases