Although sodium has traditionally been considered the most influential dietary mineral in the development of hypertension, mounting evidence implicates a potassium (K) deficit in the development of hypertension and its cardiovascular sequelae. 1 , 2 K is the main intracellular cation, and K deficit in animals and humans is associated with the development of hypertension. Young rats with a low K intake experience a deficit in cellular K that triggers the accumulation of intracellular sodium to maintain tonicity and volume. 3 The effect of K depletion on blood pressure (BP) level is revealed when sodium chloride is consumed in excess. 4
In humans, Krishna and colleagues 5 investigated the effects of dietary K restriction on BP using low‐ or normal‐K diets with usual sodium intake in normotensive men. With the low‐K diet, serum K levels declined and plasma sodium and chloride levels were unchanged; however, the average daily excretion of urinary sodium was significantly lower on the low‐K diet than on the normal‐K diet, indicating that sodium retention had resulted. BP did not change significantly in those on the normal‐K diet but increased a small but definite amount in those on the low‐K diet. Participants were then given a saline infusion, which further increased BP in those on the low‐K diet but had no effect on those consuming the normal diet. Plasma renin activity and plasma aldosterone concentrations also decreased in patients during the low K intake.
Kaplan and coworkers 6 looked at the effects of K repletion in hypertensive patients with diuretic‐induced hypokalemia (K level <3.5 mEq/L). Compared with placebo, participants receiving potassium chloride (KCl) 60 mmol/d had an average increase in serum K levels of 0.56 mmol/L and a mean decrease in diastolic BP of 5.5 mm Hg.
There is concern that chloride may minimize the antihypertensive activity of K. Potassium bicarbonate supplementation of 60 mEq/d has been shown to have a greater antihypertensive effect than a similar dose of KCl. 7 In stroke‐prone, spontaneously hypertensive rats, KCl had more of an effect on BP and the incidence of stroke than did potassium bicarbonate or potassium citrate, which attenuated the hypertension. 8
Maintenance of adequate K balance is important for hypertensive patients. Patients with high BP and normal renal function should be encouraged to consume foods enriched with K. K supplements are useful for diuretic‐induced hypokalemia, when patients cannot correct K intake by dietary means. Often, a potassium‐sparing diuretic is a more palatable alternative.
References
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