Protective effect of potassium against the hypertensive cardiac dysfunction: association with reactive oxygen species reduction.

Full 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.

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Author information

Author/s: Matsui, Hiromitsu (H); Shimosawa, Tatsuo (T); Uetake, Yuzaburo (Y); Wang, Hong (H); Ogura, Sayoko (S); Kaneko, Tomoyo (T); Liu, Jing (J); Ando, Katsuyuki (K); Fujita, Toshiro (T);

Affiliation: Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Tokyo, Japan.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Hypertension (Hypertension), published in United States. (Language: eng)

Reference: 2006-Aug; vol 48 (issue 2) : pp 225-31

Dates: Created 2006/07/21; Completed 2006/09/05; Revised 2006/11/15;

PMID: 16818802, status: MEDLINE (last retrieval date: 12/26/2008)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

Comments and Corrections

CommentIn: Hypertension. 2006 Aug;48(2):201-2. (PMID: 16818803)

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals
Blood Pressure - drug effects
Body Weight - drug effects
Dietary Supplements
Disease Models, Animal
Echocardiography
Heart Ventricles - metabolism; pathology; physiopathology
Hypertension - complications; diet therapy; physiopathology
Male

NADPH Oxidase - metabolism
Organ Size - drug effects
Potassium Chloride - administration & dosage
Potassium, Dietary - therapeutic use
Rats
Rats, Inbred Dahl
Reactive Oxygen Species - metabolism
Sodium Chloride, Dietary
Ventricular Dysfunction, Left - complications; physiopathology; prevention & control

Associated Chemicals: Potassium, Dietary (0) ; Reactive Oxygen Species (0) ; Sodium Chloride, Dietary (0) ; Potassium Chloride (7447-40-7) ; NADPH Oxidase (EC 1.6.3.1)

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