We conducted this study to determine whether physiological changes in potassium concentration affect free radical formation by vascular cells. We assessed the effects of potassium on reactive oxygen species formed by cultured endothelial and monocyte/macrophage cells or freshly isolated human white blood cells by cytochrome c reduction or luminol chemiluminescence, respectively. Reducing potassium concentration of endothelial cell media (normally 5.1 to 6.1 mmol/L) to 3.0 mmol/L exponentially increased the rate of cytochrome c reduction, up to 8.4-fold at 2 hours; raising potassium concentration to 5.5 or 7.0 mmol/L at 1 hour reduced the maximal rate of cytochrome c reduction by 86% or 93%. Subsequent studies were done 30 to 75 minutes after media change. Potassium reduced the rate of cytochrome c reduction by 49% (endothelial cells) to 55% (monocytes/macrophages) between 3.0 and 7.0 mmol/L; the greatest decrement (20% to P otassium intake (60 to 80 1 mmol/d) and urinary potassium excretion 2 are inversely related to the incidence of stroke-associated mortality in adult women. Most studies also find a significant inverse relation between potassium intake (ranges: 23 to 54, 3 Moreover, the correlation coefficient of the relation between plasma potassium and diastolic blood pressure is three times greater in young (<36 years) than in old (>49 years) patients. 26 It has been proposed that potassium antagonizes the formation of early renovascular lesions 25 thought to initiate hypertension in youth. 27Support for this hypothesis has come from animal studies in which increased dietary potassium reduces the incidence of renovascular and aortic fatty-streak lesions in rats. -29There is a highly significant inverse correlation between plasma potassium (3.0 to 5.5 mmol/L) and blood pressure in hypertensive patients less than 36 years of age. 26 Varying potassium intake from 0 to 300 mmol/d for 5 days causes a corresponding 0.8 -mmol/L change in fasting plasma potassium.11 Lowering potassium intake from 96 to 16 mmol/d for 10 days reduces fasting plasma potassium from 4.2 to 3.4 mmol/L.12 Raising potassium intake from 80 to 200 mmol/d for 8 weeks raises fasting plasma potassium from 4.2 to 4.4 mmol/L.15 High potassium meals (100 mmol) further increase plasma potassium over 4 hours, peaking 2 hours after eating at 0.6 mmol/L above fasting levels. 30 Moderate potassium meals (25 mmol) do not alter postprandial plasma potassium. 30 These studies indicate that changes in dietary potassium can alter fasting plasma potassium by at least 1 mmol/L and peak postprandial plasma potassium by more than 1.5 mmol/L.Habitual changes in potassium intake may elicit greater changes in plasma potassium. The human body contains 2460 mmol of potassium, 31 35 times the average daily adult potassium intake, most of which is excreted. 32 Animal studies have shown that body potassium stores can change by 23% and that potassium balance is not achieved weeks after potassium intake is altered.