Potassium chloride supplementation diminishes platelet reactivity in humans.
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.
Kimura
Masayuki
M
Hypertension Research Center, Cardiovascular Research Institute, University of Medicine and Dentistry of New Jersey, Newark 07103, USA.
Lu
Xiaobin
X
Skurnick
Joan
J
Awad
Girgis
G
Bogden
John
J
Kemp
Francis
F
Aviv
Abraham
A
D000244:Adenosine Diphosphate / Q000378:metabolism; D000328:Adult; D001794:Blood Pressure; D015331:Cohort Studies; D019587:Dietary Supplements; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015539:Platelet Activation / Q000187:drug effects*; D010974:Platelet Aggregation / Q000187:drug effects; D011188:Potassium / Q000652:urine; D011189:Potassium Chloride / Q000378:metabolism / Q000494:pharmacology*; D012964:Sodium / Q000652:urine
D000244:Adenosine Diphosphate; D011189:Potassium Chloride; D012964:Sodium; D011188:Potassium