POTASSIUM

Function and essentiality Potassium (K) is predominantly an intracellular cation. This compartmentalisation of K is maintained by the energy dependent cellular uptake of the element and simultaneous extrusion of sodium by the cell membrane bound enzyme Na: K adenosine triphosphatase. This process is fundamental to the cellular uptake of molecules against electrochemical and concentration gradients, to the electrophysiology of nerves and muscle, and to acid-base regulation (1, 2).


Metabolism An adult male is estimated to contain 40-50 mmol (1.6-2.0 g)/kg body weight, on which basis a 70 kg adult would contain 2800-3500 mmol (110-137 g). At least 95 per cent of this is intracellular at an activity concentration of 150 mmol/L (5.9 g/L); the residue is present in the ECF at a concentration of 3.5-5.5 mmol/L (137-215 mg/L). The total body K reflects lean tissue mass and consequently varies with muscularity.


Homeostasis The homeostasis of K is imperfectly understood and many factors are involved (see Bioavailability - not yet available). Over 90 per cent of dietary K is absorbed in the proximal small intestine. The body content is regulated by renal glomerular filtration and tubular secretion but up to 10 per cent of the daily loss can occur via the distal ileum and the colon and a small amount is lost in sweat. The glomerular filtration of K is approximately 3 per cent of the value for sodium, and amounts to only about 680 mmol/d (26.5 g/d). However, renal tubular secretion of the element, which is regulated predominantly by aldosterone, is highly efficient and the kidney is able to excrete K considerably in excess of this filtered load. As long as renal function is normal it is almost impossible to induce K excess on habitual dietary intakes. An additional, but usually less important, regulation of ECF and plasma K excess is achieved by the capacity of cells induced by glucose and insulin to take up K.


Deficiency

Potassium deficiency alters the electrophysiological characteristics of cell membranes causing weakness of skeletal muscles. The effect on cardiac muscle is reflected by electrocardiographic changes characteristic of impaired polarisation which may lead to arrhythmias and cardiac arrest. Similar changes in intestinal muscle cause intestinal ileus (loss of motility). Mental depression and confusion can also develop. Potassium is needed for lean tissue synthesis and an adequate K intake is needed to achieve effective homeostasis of sodium and renal function. Potassium deficiency arising from an inadequate dietary intake is unlikely because of the ubiquity of K in foodstuffs.

Young normotensive men on a K intake of 10 mmol/d (390 mg/d) were less able to excrete an imposed sodium excess than when they had a K intake of 90 mmol/d (3.5 g/d) (3); simultaneously their blood pressure increased. In an international study urinary K excretion, an assumed indicator of K intake, was negatively related to blood pressure as was the urinary Na:K concentration ratio (4). Potassium intakes of 65 and 100 mmol/d (2.5 and 3.9 g/d) reduce blood pressure in normotensive and hypertensive individuals and increase urinary sodium loss (5, 6). Although some studies contradict these findings it seems reasonable to ensure that habitual daily K intakes are maintained at suitable levels to ensure optimal metabolism of sodium. It has been calculated that an increase in K intakes of 60-80 mmol/d (2.3-3.1 g/d) might induce a fall of 4 mm Hg systolic blood pressure with a possible 25 per cent reduction in deaths related to hypertensions.


Requirements These are difficult to determine precisely but they can be gauged from the amount accumulated with growth and from reported urinary and faecal excretion, although the latter, of course, may represent homeostatic excretion of excessive intakes or losses incurred in maintaining sodium homeo- stasis. An additional allowance can be made for amounts lost via the skin and hair. The basal K losses of children have not been clearly defined; observed urinary excretion range from 0.7-2.3 mmol/kg/d (27-90 mg/kg/d). The amount needed for growth and lean tissue synthesis has been taken as 50 mmol (2.0 g)/kg body weight, and the Panel has used these factors with an allowance for integuemental and faecal losses in estimating DRVs for K factorially up to 18 years of age.


Intakes In the Dietary and Nutritional Survey of British Adults mean K intakes were 3187 and 2434 mg/d (82 and 62 mmol/d) in men and women respectively and mean 24 urinary K excretions were 3000 mg (77 mmol) and 2420 mg (62 mmol) respectively (7). Potassium is particularly abundant in vegetables, potatoes, fruit (especially bananas) and juices. Dietary trends with decreased consumption of vegetables and fruit and increased consumption of foods with sodium based preservatives and other additives favour reduced K and increased sodium intakes.


Guidance on high intakes Reported K intakes by Western populations are in the range of 40-150 mmol/d (1.6-5.9 g/d). Intakes above 450 mmol (17.6 g) may induce symptomatic hyperkalaemia in some individuals and would represent a threshold for acute toxicity but such amounts would only be achieved by supplementation and on usual dietary intakes toxicity is unlikely (8).


References

1 Pitts R F. Physiology of the Kidney and Body Fluids 2nd Ed. Chicago: Year Book Medical Publishers 1968.

2 Patrick J. Assessment of body potassium stores. Kidney Int 1977; 11: 476-490.

3 Krishna G G, Miller E, Kapoor S. Increased blood pressure during potassium depletion in normotensive men. New Engl J Med 1989; 320: 1177-1182.

4 Intersalt Cooperative Research Group. Intersait: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Br Med J 1988; 297: 319-328.

5 Rose G. Desirability of changing Potassium intake in the community. In: Whalton P el al, eds. Potassium in Cardiovascular and Renal Disease. New York: Marcel Dekker, 1986; 411-416.

6 Matiou S M, Isles C G, Higgs A et al. Potassium supplementation in Blacks with mild to moderate essential hypertension. J Hyperten 1986; 4: 61-64.

7 Gregory J, Foster K, Tyler H, Wiseman M. The Dietary and Nutritional Survey of British Adults. London: HMSO, 1990.

8 National Academy of Sciences. Recommended Dietary Allowances 9th Ed. Washington DC: National Academy of Sciences, 1980.