Published Online
on October 25, 2004

A more recent version of this article appeared on December 1, 2004

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Submitted on June 21, 2004
Revised on July 12, 2004

Potassium Chloride Supplementation Diminishes Platelet Reactivity in Humans

Masayuki Kimura; Xiaobin Lu; Joan Skurnick; Girgis Awad; John Bogden; Francis Kemp; and Abraham Aviv^*

From the Hypertension Research Center, Cardiovascular Research Institute (M.K., X.L., G.A., A.A.), and the Department of Preventive Medicine and Community Health (J.S., J.B., F.K.), University of Medicine and Dentistry of New Jersey, Newark.

^* To whom correspondence should be addressed. E-mail: avivab{at}umdnj.edu.

Abstract--The prevalence of occlusive stroke is inversely correlated with potassium intake. We explored the hypothesis that a high potassium intake attenuates platelet reactivity, as expressed in ADP-evoked platelet aggregation. We studied healthy men (n=31) and women (n=42), blacks (n=33) and whites (n=40). In this cohort, we supplemented the habitual intake of 17 men and 21 women with 60 mmol KCl/70 kg body weight per day for 3 days and maintained 14 men and 21 women on their habitual intake. We then compared the change in ADP concentration causing 50% of the maximal initial rate (EC₅₀) of platelet aggregation in the potassium-supplemented versus control groups. Potassium supplementation attenuated platelet reactivity, expressed by an increase in EC₅₀ of platelet aggregation (P=0.0005), which was primarily attributable to an increase in EC₅₀ in whites (P=0.0004). Urinary potassium excretion was significantly lower in blacks than in whites under basal conditions and after potassium supplementation. We conclude that potassium supplementation diminishes platelet reactivity, a phenomenon that provides a link between platelet biology and occlusive stroke.

Key words: stroke • cardiovascular disease • atherosclerosis

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