INTRODUCTION — A low dietary intake of potassium may increase the blood pressure, and potassium supplementation almost always lowers elevated blood pressure. The data demonstrating these associations, as well as the potential mechanisms, will be reviewed here. The approach to patients who present with concurrent hypertension and hypokalemia, and the clinical features of primary aldosteronism, are discussed separately. (See "Diagnosis of primary aldosteronism" and "Pathophysiology and clinical features of primary aldosteronism".)
POTASSIUM INTAKE AND BLOOD PRESSURE — The level of potassium intake can affect blood pressure. The effect varies with the direction (low potassium intake raises the blood pressure, and high potassium intake lowers the blood pressure) and magnitude of change in potassium intake.
Low-potassium diet — Low dietary potassium intake (below 40 mEq/day [1.5 g/day]) has been associated with an elevation in blood pressure and an increased risk of stroke [1-4], as well as an increase in risk of chronic kidney disease [5]. The following observations are illustrative:
●In two different studies, one in healthy normotensive men [6] and one in patients with primary hypertension (formerly called essential hypertension) [7], potassium restriction from a normal intake of 80 to 90 mEq/day down to 10 to 18 mEq/day led to a statistically significant 4 to 5 mmHg increase in systolic blood pressure. The increase in blood pressure may have been mediated in part by sodium retention.
●In a meta-analysis of 11 cohort studies and nearly 250,000 individuals, a 1.64 g (42 mmol)/day higher potassium intake was associated with a 21 percent lower risk of stroke [2].
In addition to the adverse effects of low dietary potassium intake, the ratio of dietary sodium-to-potassium intake can also influence blood pressure [8]. In a report from the Dallas Heart Study, each three-unit increase in the urine sodium-to-potassium ratio, which can reflect increased sodium intake and/or reduced potassium intake, was associated with a 1.6/1 mmHg elevation in blood pressure [9]. A higher sodium-to-potassium intake ratio is also associated with an increase in overall cardiovascular mortality [10,11].
High-potassium diet — In contrast to the rise in blood pressure associated with a low-potassium diet, potassium supplementation lowers the blood pressure significantly in hypertensive patients and insignificantly in normotensive patients. The magnitude of change has been illustrated in systematic reviews that included meta-analyses of both randomized trials and cohort studies [1,12]. The following findings were noted in the larger of these studies [1]:
●In a meta-analysis of 16 randomized trials in hypertensive patients, increased potassium intake significantly reduced systolic blood pressure by a mean of 5.3/3.1 mmHg. By contrast, the reduction in blood pressure was small (0.1/0.6 mmHg) and not statistically significant in three trials in normotensive subjects.
●When a subgroup analysis was performed according to achieved potassium intake, patients with an increase to 90 to 120 mEq/day had the largest reduction in blood pressure (7.2/4.1 mmHg).
In another meta-analysis, the effect of potassium supplementation on blood pressure was greater in Black patients than in White patients [13]. Urinary potassium excretion in Black patients is consistently less than in White patients [14,15]. This difference is due in part to less dietary potassium intake in Black patients [15,16].
In addition to the lower rate of potassium intake, another factor that may contribute to the increased predisposition to hypertension in Black patients is a relative increase in the activity of the Na-K-2Cl cotransporter in the luminal membrane in the thick ascending limb of the loop of Henle (figure 1) [14]. This defect could contribute to the decreased plasma renin activity, lower rate of urinary potassium excretion, and increased salt sensitivity often seen in Black patients.
Clinical implications — Based upon the above observations, it has been proposed that hypertensive patients with normal or near-normal kidney function should be encouraged to maintain a high potassium intake from fresh fruits and vegetables [17]. Dietary counseling is the usual approach to increasing potassium intake.
Potassium chloride supplements can also be used, particularly if the serum potassium concentration is low. However, if there is no apparent cause for the hypokalemia (eg, diuretic therapy, gastrointestinal losses), the patient should be evaluated for the disorders that are associated with both hypertension and hypokalemia. These include primary aldosteronism, renovascular disease, and Cushing's syndrome. (See "Diagnosis of primary aldosteronism" and "Causes of hypokalemia in adults", section on 'Diuretics'.)
Few Americans achieve the recommended level of potassium intake. In a report from the National Health and Nutrition Examination Survey (NHANES) III, the average daily potassium intake in adults was 74 to 82 mEq (2.9 to 3.2 g) in men and 54 to 59 mEq (2.1 to 2.3 g) in women [18]. Only 10 percent of men and less than 1 percent of women had a daily potassium intake of 120 mEq (4.7 g) or more.
We do not recommend potassium supplementation or a high-potassium diet to attain these goals in patients at risk for hyperkalemia due, for example, to therapy with angiotensin inhibitors, potassium-sparing diuretics, or underlying chronic kidney disease.
MECHANISMS — There are several mechanisms by which potassium intake affects hypertension and vascular disease [11,19,20]. In particular, low potassium intake may reduce sodium excretion due in part to effects of potassium deficiency on the activity of the chloride-sensitive WNK (With-No-Lysine) kinase pathway, resulting in activation of the thiazide-sensitive NaCl cotransporter [21,22]. Conversely, high potassium intake increases sodium excretion. Potassium "sensing" via basolateral potassium (K+) channels in the distal convoluted tubule plays a key role in these pathways [23]. Potassium also modulates the renin angiotensin system, which is upregulated in the setting of hypokalemia [20]. Finally, hypokalemia causes vascular calcification and promotes arterial stiffness through induction of autophagy and promotion of vascular smooth muscle calcification [24].
Relation to sodium excretion — The relationship between potassium and blood pressure appears to be due in part to changes in sodium excretion, as noted above [9]. Sodium excretion is diminished by hypokalemia or a low-potassium diet and increased with potassium supplements, apparently through changes in sodium reabsorption in the proximal tubule and/or loop of Henle [25]. (See 'Potassium intake and blood pressure' above and "Hypokalemia-induced kidney dysfunction", section on 'Increased sodium reabsorption'.)
Role of chloride intake — Chloride is an important determinant of the rise in blood pressure in salt-sensitive forms of hypertension. By comparison, dietary potassium (eg, from fruits and vegetables) is primarily associated with organic anions such as citrate, not chloride. (See "Salt intake, salt restriction, and primary (essential) hypertension".)
The relative efficacy of potassium bicarbonate or potassium citrate (citrate is metabolized to bicarbonate) supplements and potassium chloride supplements has been directly evaluated in randomized crossover trials of patients with hypertension [26,27]. The bicarbonate, citrate, and chloride preparation all produced a similar reduction in blood pressure. Thus, the available evidence does not support the accompanying anion being important in the effect of potassium on blood pressure.
SUMMARY
●Maintenance of adequate potassium intake or the administration of potassium supplements usually lowers the blood pressure, particularly in Black patients and in patients who are not sodium restricted. Furthermore, a higher potassium intake reduces the risk of stroke. (See 'Potassium intake and blood pressure' above and 'Relation to sodium excretion' above.)
●The mechanism by which potassium reduces blood pressure is not clear. (See 'Mechanisms' above.)
●Some experts suggest that hypertensive patients should consume at least 120 mEq (4.7 g) of dietary potassium/day provided they do not have a predisposition to hyperkalemia. This level of potassium intake can be achieved preferably with dietary counseling. (See 'Clinical implications' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Norman M Kaplan, MD, who contributed to an earlier version of this topic review.
