Uses of this Supplement
Diabetes Mellitus
Myocardial Infarction
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  Drugs that Interact
Angiotensin-Converting Enzyme (ACE) Inhibitors
Beta-Adrenergic Blockers
Nonsteroidal Anti-inflammatory Drugs (NSAIDs)
Sulfamethoxazole-containing Medications
Trimethoprim-containing Medications
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Look Up > Supplements > Potassium
Dietary Sources
Commercial Preparations
Therapeutic Uses
Dosage Ranges and Duration of Administration
Side Effects/Toxicology


Potassium is the principal cation in intracellular fluid with a concentration of 140 mmol/L. The extracellular fluid potassium concentration is only 3.5 to 5.5 mmol/L. Together with sodium, the principal cation of the extracellular fluid, potassium maintains the potential difference across cell membranes. The importance of potassium's contribution to this function is best demonstrated by the consequences of elevations and depletions of potassium in extracellular fluid on cardiac function. Both conditions result in abnormal depolarization and repolarization of cardiac cells, leading to potentially fatal cardiac arrhythmias and conduction disturbances.

Other physiologic functions in which potassium plays a role include energy metabolism, membrane transport, normal water balance, acid–base balance, and osmotic equilibrium. The relationship of potassium and sodium is essential to good health, with a ratio of dietary potassium to sodium recommended at 5:1.

Recent studies have provided strong evidence that potassium may have an antihypertensive function. A meta-analysis of 33 randomized controlled clinical trials with approximately 2,600 participants demonstrated that potassium supplementation was associated with a significant reduction in mean systolic and diastolic blood pressure. The mechanisms behind the blood pressure–lowering effects of potassium include effects on natriuresis, the renin-angiotensin-aldosterone system, direct vasodilatory functions, baroreflex sensitivity, and catecholaminergic functions. Potassium also appears to improve glucose tolerance.

Other studies suggest that there may be a role for potassium together with glucose and insulin in the reduction of acute myocardial infarction (MI) mortality. Glucose-insulin-potassium (GIK) treatment was shown to decrease acute MI mortality by itself or in combination with thrombolytic therapy, revascularization procedures, or both. A possible mechanism of GIK action is decrease of both circulating levels of free fatty acids (FFA) and myocardial uptake of FFA.

Studies have revealed that the elderly are at high risk for hyperkalemia. The aging process alters normal renal function, leading to an inhibition of normal potassium excretion. In this setting of impaired renal function, several drugs which are commonly prescribed to the elderly can further alter the kidney's ability to excrete potassium, leading to hyperkalemia and a potentially life-threatening situation.

Dietary Sources

The richest dietary sources of potassium are fresh unprocessed food including meats and fish, vegetables (especially potatoes), fruits (especially avocados and bananas), and citrus juices. Ample potassium can be obtained by a varied diet with adequate intake of milk, meats, cereals, vegetables, and fruits.


Potassium is a metallic element of the alkali group with an atomic weight of 39 and atomic symbol of K. As described in the overview section of this monograph, it is the chief intracellular cation; 98% of total body potassium is found in the intracellular fluid.

Commercial Preparations

Potassium supplements are usually available in the form of potassium salts or potassium bound to mineral chelates. These include the following:

  • Potassium acetate
  • Potassium bicarbonate
  • Potassium chloride
  • Potassium citrate (effervescent)
  • Potassium gluconate

Potassium is also sometimes included in multivitamin preparations.

Therapeutic Uses
  • Hypokalemia
  • Hypertension
  • Reduce mortality associated with acute MI (used in combination with glucose and insulin)
  • Glucose intolerance
  • Stroke prevention
  • Cardiac arrhythmias
  • Muscle weakness
  • Diabetes mellitus

Dosage Ranges and Duration of Administration

The average potassium intake estimated by the National Research Council is as follows:

  • In infants: 780 mg/day
  • In children: 1,600 mg /day
  • In adults: 3,500 mg/day

There is no recommended increased intake of potassium during pregnancy and lactation.

Side Effects/Toxicology

Side effects from prescribed use include the following:

  • Gastrointestinal (stomach pain, nausea, vomiting, diarrhea, flatulence)
  • Cardiovascular (bradycardia)
  • Metabolic, endocrine (hyperkalemia)
  • Respiratory (weakness, difficult breathing)
  • Local tissue necrosis with extravasation

Toxic effects due to overdose include the following:

  • Muscle weakness
  • Lethargy
  • Gastric hypomotility
  • Paralysis
  • Cardiac arrhythmia
  • Conduction disturbances
  • Death


Use with caution in patients with renal insufficiency. Should not be used in patients with severe renal impairment. Because renal function declines with age, the elderly are at high risk of renal insufficiency. Care should be taken when prescribing potassium supplements to the elderly.


Medications that may diminish potassium levels include corticosteroids, amphotericin B, antacids, loop diuretics, thiazide diuretics, and insulin. Please refer to the depletions monographs related to these medications for additional information.

Angiotensin-Converting Enzyme (ACE) Inhibitors

ACE inhibitors may produce hyperkalemia, particularly when used in combination with nonsteroidal anti-inflammatory drugs (NSAIDs), potassium-sparing diuretics, potassium supplements, potassium-containing salt substitutes, and in patients with autonomic neuropathy, adrenal insufficiency, renal impairment, and diabetes mellitus (Howes 1995; Shionoiri 1993). For this reason, potassium supplements may not be warranted in patients taking these medications; serum potassium levels should be monitored closely.

Beta-Adrenergic Blockers

Beta-adrenergic blockers may elevate potassium levels by promoting a redistribution of this electrolyte (Preston et al. 1998). Potassium levels should be monitored in patients taking these medications, particularly in patients with compromised renal function.


Cyclosporine may induce hyperkalemia by decreasing renal excretion of potassium and interfering with aldosterone production or secretion (Preston et al. 1998). Potassium levels in patients on cyclosporine therapy, particularly those with renal insufficiency, should be monitored carefully.


Hypokalemia increases the risk of cardiac glycoside toxicity (Whang et al. 1985). Normal levels of potassium should be maintained during digoxin treatment.


Heparin may contribute to hyperkalemia by impairing renal excretion of potassium as a result of interference with aldosterone production or secretion (Preston et al. 1998). Serum potassium levels should be monitored in patients on heparin therapy, especially if potassium supplements are added to the medication regimen.

Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

NSAIDs can affect renal function and decrease potassium excretion (Brater 1999). Hyperkalemia can occur in patients with mild renal insufficiency or normal renal function. Ibuprofen may increase the risk for renal insufficiency and cause hyperkalemia in patients that are over 76 years old, on certain diuretic therapy, or who have cirrhosis and renal vascular disease (Blackshear et al. 1983; Poirier 1984; Whelton, et al. 1990). Individuals taking NSAIDs should avoid potassium supplements.

Trimethoprim; Co-Trimoxazole

Standard doses of trimethoprim monotherapy as well as trimethoprim combined with sulfamethoxazole have been shown to cause hyperkalemia in a significant number of patients treated for various infections (Alappan et al. 1996; Perazella 2000). Patients treated with these medications should be closely monitored for hyperkalemia, especially those with renal insufficiency (Alappan et al. 1996).


Alappan R, Perazella MA, Buller GK, et al. Hyperkalemia in hospitalized patients treated with trimethoprim-sulfamethoxazole. Ann Intern Med. 1996;124(3):316-320.

Apstein C. Glucose-Insulin-Potassium for acute myocardial infarction: remarkable results from a new prospective, randomized trial. Circulation. 1998;98:2223-2226.

Ascherio A, Rimm EB, Hernan MA, et al. Intake of potassium, magnesium, calcium, and fiber and risk of stroke among U.S. men. Circulation. 1998;98:1198-1204.

Blackshear JL, Davidman M, Stillman MT. Indentification of risk for renal insuffciency from nonsteroidal anti-inflammatory drugs. Arch Intern Med. 1983;143(6):1130-1134.

Brancati FL, Appel LJ, Seidler AJ, Whelton PK. Effect of potassium supplementation on blood pressure in African Americans on a low-potassium diet. Arch Intern Med. 1996;156:61-72.

Brater DC. Effects of nonsteroidal anti-inflammatory drugs on renal function: focus on cyclooxygenase-2-selective inhibition. Am J Med. 1999;107(6A):65S-70S.

Ganong WF. Review of Medical Physiology. 18th ed. Stamford, Conn: Appleton & Lange; 1997:677.

Howes LG. Which drugs affect potassium? Drug Saf. 1995 Apr;12(4):240-244.

Luft F, Ekhard ZE, Filer LJ, eds. Present Knowledge in Nutrition. 7th ed. Washington, DC: ILSI Press; 1996:272-276.

Mahan LK, Arlin MT, eds. Krause's Food, Nutrition, and Diet Therapy. 8th ed. Philadelphia, Pa: WB Saunders Co.; 1992:147, 390.

National Research Council: Recommended Dietary Allowances. 10th ed. Washington, DC: National Academy Press; 1989:255-257.

Perazella MA. Trimethoprim-induced hyperkalemia: clinical data, mechanism, prevention and management. Drug Saf. 2000;22(3):227-236.

Poirier TI. Reversible renal failure associated with ibuprofen: case report and review of the literature. Drug Intell Clin Pharm. 1984;18(1):27-32.

Preston RA, Hirsh MJ MD, Oster, JR MD, et al. University of Miami Division of Clinical Pharmacology therapeutic rounds: drug-induced hyperkalemia. Am J Ther. 1998 Mar; 5(2):125-132.

Sacks FM, Willett WC, Smith A, et al. Effect on blood pressure of potassium, calcium, and magnesium in women with low habitual intake. Hypertension. 1998;31(1):131-138

Shionoiri H. Pharmacokinetic drug interactions with ACE inhibitors. Clin Pharmacokinet. 1993 Jul;25(1):20-58.

Singh RB, Singh NK, Niaz MA, Sharma JP. Effect of treatment with magnesium and potassium on mortality and reinfarction rate of patients with suspected acute myocardial infarction. Int J Clin Pharmacol Thera. 1996;34:219-225.

Suter PM. Potassium and hypertension. Nutrition Reviews. 1998;56:151-133.

Whang R, Oei TO, Watanabe A. Frequency of hypomagnesia in hospitalized patients receiving digitalis. Arch Intern Med. 1985;145(4):655-656.

Whelton, A, Stout RL, Spilman PS, Klassen DK. Renal effects of ibuprofen, piroxicam, and sulindac in patients with asymptomatic renal failure. A prospective, randomized, crossover comparison. Ann Intern Med. 1990;112(8):568-576.

Young DB, Lin H, McCabe RD. Potassium's cardiovascular protective mechanisms. Am J Physiology. 1995;268(part 2):R825-R837.

Copyright © 2000 Integrative Medicine Communications

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