Role of potassium in the pathogenesis of hypertension

Epidemiologic studies from divergent geographic locations consistently demonstrate an inverse correlation between potassium intake and the prevalence of hypertension. Studies in experimental animals showed a varied blood pressure response to alterations in potassium intake. Spontaneously hypertensive rats and rats with renovascular hypertension manifest a hypotensive response to both potassium depletion and potassium supplementation. In contrast, potassium depletion induced by chronic mineralocorticoid administration is associated with an increase in blood pressure. Potassium supplementation in hypertensive subjects lowers blood pressure. Amelioration of diuretic-induced hypokalemia with potassium supplementation enhances the hypotensive effect of diuretics. Potassium depletion induced by dietary potassium restriction elevates blood pressure in normotensive and hypertensive subjects maintained on a normal sodium intake. Potassium depletion in humans is accompanied by sodium retention and calcium depletion. The hypertensive response to potassium depletion and the hypotensive response to potassium supplementation do not manifest if sodium intake is kept low. Sodium retention, altered response to vasoactive hormones, direct vasoconstrictive effects of hypokalemia, and calcium depletion may all contribute to blood pressure elevation during potassium depletion.