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(Hypertension. 2006;48:225.)
© 2006 American Heart Association, Inc.

Original Articles

Protective Effect of Potassium Against the Hypertensive Cardiac Dysfunction

Association With Reactive Oxygen Species Reduction

Hiromitsu Matsui; Tatsuo Shimosawa; Yuzaburo Uetake; Hong Wang; Sayoko Ogura; Tomoyo Kaneko; Jing Liu; Katsuyuki Ando; Toshiro Fujita

From the Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Japan.

Correspondence to Toshiro Fujita, Department of Nephrology and Endocrinology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku Tokyo, 113-8655, Japan. E-mail fujita-dis{at}h.u-tokyo.ac.jp

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.

Key Words: sodium • blood pressure monitoring • cardiac function • heart failure • oxidative stress • potassium

Related Article:

Potassium Depletion and Diastolic Dysfunction

David B. Young
Hypertension 2006 48: 201-202. [Full Text] [PDF]

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