Anaesth. Intens.

Care (1977), 5, 317

POTASSIUM METABOLISM
J. R. STOCKIGT*
Alfred Hospital, Melbourne

SUMMARY
In man, mechanisms for potassium excretion are complex and highly developed, while
potassium conservation is potentially inadequate. Potassium balance is regulated by
alterations in excretion in the distal renal tubule, where mineralocorticoid hormones and
N a-K ATPase are the major regulating factors. The distribution of potassium across cell
membranes is influenced by changes in acid-base stattts, by pancreatic hormones and by the
autonomic nervous system. Potassium stimulates insulin and aldosterone secretion and
increases Na-K ATPase in the distal nephron, so promoting its own redistribution or excretion.
Emergency management of hyperkalaemia is best effected by promoting cell-entry of potassium,
rather than renal excretion. The speed of replacement of deficits is always limited by the
small extracellular potassium pool.

INTRODUCTION In man, mechanisms which prevent potassium

Potassium is the major intracellular cation
and determinant of membrane polarization;
consequently its plasma concentration must be
precisely regulated, irrespective of total body
content. This is achieved both by change in
distribution across cell membranes and by
modification of renal excretion. Because intake,
absorption and proximal renal reabsorption do
not show regulatory variation, total body
potassium balance is controlled by appropriate
changes in excretion in the distal portion of the
nephron.
Potassium homeostasis can be disturbed by
renal impairment, disturbances of acid-base
balance, excessive tissue breakdown, abnormal
routes of loss, aberrations of sodium balance
and mineralocorticoid abnormalities. Potas-
sium overload is opposed by several factors
which are directly responsive to an increase in
its blood level. A rise in plasma potassium
can directly stimulate aldosterone production,
insulin secretion and sodium-potassium ATPase
in the renal medulla; each of these factors
either promotes the movement of potassium
into cells, or its excretion in urine.
* M.D., F.R.A.C.P., Deputy Director, Ewen Downie
Metabolic Unit.
Address for reprints: Dr. J. R. Stockigt, Ewen
Downie Metabolic Unit, Alfred Hospital. Prahran,
3181, Victoria, Australia.
overload are much more highly developed
than those which prevent depletion, perhaps
because feral man ingested a diet high in
potassium and low in sodium. This background
equips us poorly for the present day high-sodium,
low-potassium environment (Meneely and
Battarbee 1976).
This review will summarize recent advances
in our understanding of the multiple mechanisms
which regulate potassium balance. The conse-
quences of potassium imbalance will not be
considered fully, but the pathologic or thera-
peutic significance of the major potassium
regulating mechanisms will be shown by clinical
examples. The review is necessarily incomplete;
further information is available from other
sources (Schultze 1973, Lowenstein 1973,
Vaughan and Lunn 1973, Brenner and Berliner
1973, Stockigt 1977, Kunau and Stein 1977).
HANDLING OF POTASSIUM LOADS
The multiple mechanisms which oppose
potassium overload are summarized in Figure l.
In the small bowel lumen, the potassium content
of ingested food rapidly approaches the plasma
concentration (Phillips and Summerskill 1967).
Absorption from small bowel is passive, leading
to movement of ingested potassium into an
extracellular space which contains less than
2% of total body potassium. Because
this pool is no larger than daily intake, potent

Anaesthesia and Intensive Care, Vol. V, No. 4, November, 1977

318
defences are essential to prevent lethal hyper-
kalaemia after oral or parenteral potassium
loads. \Vhen a potassium load is given
parenterally, the speed of administration is
more critical than the amount, because the
small extracellular pool can e~'iily be overloaded.
The ability to survive acute potassium
loads is described ~" potassium tolerance, while
adaptation describes the increased tolerance
which is induced by prior high potassium
INGESTION OF HIGH K LOAD
/ i ~
INSULIN ALDOSTERONE
l/~l
REDISTRIBUTION RENAL EXCRETION
CELL ENTRY
? Beta, ADRENERGIC MECHANISM
FIGL'RE I.-Summary of the factors which oppose
hyperkalaemia after acute potassium loads. Chronic
high potassium intake increases the efficiency of
these mechanisms, thereby increasing tolerance to
acute loads.
intake. Tolerance occurs mainly because of
greater renal excretion, but redistribution into
cells may also be increased (Wright et al. I n7l,
Alexander and Le\'insky .HJti~, Epstein et al.
1n7;"».
Sudden changes of pot~'isium intake are
uncommon in man, hut hypokalaemic muscle
paralysis has been reported in ::\ew Guineans
after migration from ,L region of high to low
potassiulll intake (Duggin and Price 1H7.!).
Hypokalaemic paralysis occurred within the
first two months after change from a highland
diet low in sodium and high in potassiulll, to a
coastal diet in which the sodium: potassium
ratio W,L'i reversed. This suggests that
mechanisms which alter potassium excretion
may be slow to change.
There is now good evidence that pancreatic
hormones play an important part in acute
redistribution of potassium loads by insulin-
induced entry of glucose and potassiulll into
cells (Santeusanio et al. 1H7:)). Acute potassium
tolerance studies showed poor sun'ival of
pancreatectomized dogs following large acute
infusions of pot~ssium, but tolerance was
restored by infusion of insulin and glucagon,
suggesting that disposal was dependent on
pancreatic hormone,.; (Hiatt, Yamakawa and
J. R. STOCKIGT
Davidson 1974). It is notable that potassium
stimulates release of both insulin and glucagon
(Santeusanio et al. 1973), so as to promote
K + removal from extracellular fluid without
major change in blood sugar (Figure 2). A
change in plasma potassium, well within the
physiologic range, stimulates insulin secretion
in normal subjects, suggesting an important
role for this mechanism in normal physiology
(Dluhy, Axelrod and Williams In72). While
it is usually presumed that the fall in potassium
is the result of glucose entry into cells, the
studies of Zierler ()!166) suggest that potassium
influx (or diminished efflux) may be a direct
Na·K ATPase
result of insulin action. Paradoxical glucose-
induced hyperkalaemia has been reported in
diabetic patients, who lack an appropriate
glucose-induced insulin response (Goldfarb et al.
In76), while potentially dangerous hypokalaemia
may occur during insulin-induced hypoglycaemia
(Strakosch, Stiel and Gyory ] 976).
K LOAD
~ RISE IN SERUM K
/~
INSULIN RELEASE GLUCAGON RELEASE
j ~ t t/
CELL ENTRY OF K GLUCOSE
FIGURE ~.-Potassiulll stimulates release of both
pancreatic insulin ancl glucagon. Insulin prorllotes
cell uptake of potassium, while glucagon stabilizes
blood sugar.
The autonomic nervous svstem is also
important in potassium distribution across
cell melllbranes. Adrenaline has a biphasic
effect on plasllla potassium, with an initial
alpha-adrenergic increase, followed lJy a more
sustained beta-mediated hypokalaemic effect.
Concurrent adrenaline infusion during potassium
loading has been shown to have a protective
effect against otherwise lethal hyperkalaemia
(Lockwoocl and LUIll J97.!). This effect, which
was indCjwndent of pancreatic insulin secretion,
could he blocked hv beta., and non-selective
beta hlockade, hut· not Gy betal hlockade.
Prevention of attacks of hyperkalaemic periodic
paralysis has recently been reported by use of
the beta 2 agonist, Salbutamol (Wang and
Anaesthesia and Jlltensive Care, Va!. V, No. 4, November, 1977
 POTASSIUM METABOLISM
Clausen 1976), further supporting the existence
of an autonomic potassium-lowering mechanism.
Isoproterenol has been shown to lower plasma
potassium in dogs by an effect independent
of pancreatic hormones (Pettit and Vick 1974),
while alpha adrenergic activity increased
potassium. The ganglion blocker, Trimetaphan
has been shown to lower serum potassium
during intraoperative hypotension (Fahmy 1976).
THE KIDNEY AND POTASSIUM
The kidney is the dominant organ in main-
taining normal potassium balance. I ts very
large excretory reserve is demonstrated by
the ability of remaining nephrons to excrete
potassium in excess of the amount filtered in
chronic renal insufficiency. Different parts of
the nephron handle potassium in different
ways, with major regulatory function confined
entirely to the distal convoluted tubule and
collecting ducts (Figure 3).
85-90% REABSORPTION
ACTIVE, NON REGULATORY
REGULATED SECRETION OR
REABSORPTION
~
Cl - DEPENDENT
REABSORPTION
N,-KAll',"
PASSIVE MOVEMENT
FIGURE 3.-Summary of potassium movement in
different parts of the nephron. Regulation of
excretion occurs only in the distal tubule and
collecting ducts.
In the proximal convoluted tubule 85-90%
of filtered potassium is reabsorbed and some
further reabsorption occurs in the thick section
of Henle's loop. Proximal reabsorption does
not show any regulatory variation in different
states of potassium balance, so that urinary
excretion may vary lOO-fold with fairly constant
amounts of potassium entering the early distal
tubule. It is in the distal tubule that mineralo-
corticoid hormones have their major action,
but potassium excretion is also influenced by
the state of acid-base balance, by the activity
of sodium potassium ATPase in the collecting
Anaesthesia and Intensive Care, Vol. V. No. 4, November. 1977
319
ducts and by the rate of flow along the distal
convoluted tubule-a factor markedly dependent
on proximal tubular sodium reabsorption.
These four major determinants of potassium
excretion will be briefly summarized:
(a) Mineralocorticoid Hormones. Aldosterone,
the major mineralocorticoid in man, is responsive
to sodium restriction, but a rise in plasma
potassium is also a potent and specific stimulus
to aldosterone production, by an action quite
independent of the renin-angiotensin system.
A rise in plasma potassium of less than
o·5 mmoljl will increase aldosterone secretion,
while prior high potassium intake magnifies
the aldosterone response to acute loads (Dluhy
et al. 1972).
The importance of adrenal corticosteroids in
potassium homeostasis is well-known, as in the
hyperkalaemia of Addisonian crisis. However,
potassium excess is a late feature of Addison's
disease and is uncommon until renal function
and acid-base balance are disturbed (Black 1972).
I t is clear that factors other than mineralocor-
ticoid hOlmones are involved in potassium
excretion, because Addisonian subjects main-
tained on fixed mineralocorticoid replacement
with 0·2 mg of 9 cx-fluorohydrocortisone daily,
were able to increase urinary potassium from
40 to 170 mmoljday when intake was increased
from 60 to 200 mmoljday (Miller et al. 1975).
It has been widely stated that sodium and
potassium ions exchange in the distal convoluted
tubule, but this view is probably false. Micro-
puncture studies have shown that distal tubular
reabsorption of sodium is always much greater
than combined secretion of potassium and
hydrogen (Malnic, Klose and Giebisch 1966).
Furthermore, sodium reabsorption occurs pre-
dominantly in the early distal tubule, while
maximum potassium secretion occurs in the
late distal tubule.
The action of mineralocorticoid hormones to
promote potassium excretion, is summarized in
Figure 4. The tubular lumen becomes progres-
sively more electronegative in the late distal
tubule and this favours potassium movement
into the lumen. Aldosterone appears to increase
potassium entry from peritubular fluid into
the distal convoluted tubule cells by an active
mechanism, in addition to its effect to enhance
luminal permeability to potassium (Wiederholt,
Agulian and Khuri 1974).
(b) Sodium-potassium ATPase. Silva et al.
(1975) have reported that an increase in the
activity of this enzyme enables the isolated,
320
perfused kidneys from potassium-loaded rats to
excrete up to three times the amount of potassium
filtered at the glomerulus. The activity of
this enzyme in the renal papilla was directly
induced by potassium, while gluco- and mineralo-
corticoid, and prior sodium restriction were
inactive at this site. This mechanism appears
to be most important in producing the marked
increase in potassium excretion per nephron
in renal insufficiency.
ALDOSTERONE
/"M}Hm. ~
ACTIVE Ne ACTIVE K TRANSPORT
REABSORPTION
/ vation is not highly developed in man. Sevele
INCREASING LUMINAL NEGATIVITY
FIGURE 4.-Action of aldosterone in the distal renal
tubule to promote active potassium transport from
peritubular fluid and increased potassium perme-
ability of the luminal cell surface. The lumen
becomes progressively more electronegative because
of active sodium reabsorption, so that maximum K+
transport occurs in the late distal tubule.
(c) Distal tubular flow. Because the potassium
gradient across the wall of the distal renal
tubule is independent of distal tubular flow
rate, a high flow rate will result in more excretion
than a low flow rate (Khuri et al. 1975). Distal
urine flow diminishes in states of sodium
deficiency, or volume depletion, where proximal
tubular sodium reabsorption is more complete.
This is the probable explanation for the dimin-
ished mineralocorticoid effect on potassium
excretion during severe sodium restriction.
Hence, the kaliuretic effect of fixed excess of
mineralocorticoid, is increased during liberal
sodium intake and diminished by sodium
restriction. Consequently, sodium restriction
is critical in achieving potassium repletion
in both primary and secondary mineralo-
corticoid excess.
(d) Acid-base balance. A hydrogen ion deficit
will increase intracellular potassium in many
cells, including the distal renal tubule, and
J. R. STOCKIGT
this is the most likely explanation for the
short-term inverse relationship between urinary
potassium and hydrogen ion excretion.
However, the long-term renal responses to
acid-base disturbances are more complex and
depend on distal sodium and anion loads rather
than on a simple inverse relationship between
H + and K +. Sustained respiratory alkalosis
produces a transient increase in potassium
excretion, but severe chronic urinary potassium
loss does not occur. However, chronic metabolic
alkalosis results in severe, progressive urinary
potassium depletion. These complex changes
have been well reviewed by Gennari and Cohen
(1975).
POTASSIUM CONSERVATION
In contrast to the multiple excretory
mechanisms outlined above, potassium conser-
potassium lack is rare in natural diets, but
contemporary preparation of food by prolonged
boiling markedly reduces potassium content and
creates an environmental stress, which, together
with potent modern pharmacology, creates
a serious danger of deficiency. Investigation
of the effect of pure potassium lack is difficult,
because food-deprivation results in catabolic
release of intracellular potassium. During
severe isocaloric potassium restriction urine
potassium falls to levels lower than the plasma
concentration-evidence for net renal
reabsorption. However, bowel loss continues,
and a progressive deficit of up to 400 mmol
may develop over 20 days, associated with
definite hypokalaemia (Squires and Huth 1959).
This progressive loss of about 15% of total
body potassium is in marked contrast to the
very efficient conservation possible for sodium.
In subjects who are stressed or ill, urine
potassium conservation is probably even less
effective than in normal subjects.
ASSESSMENT OF POTASSIUM STATUS
Because electrocardiographic monitoring
reflects minute-to-minute changes in trans-
membrane potassium gradient (Surawicz 1967),
it is irreplaceable where rapid fluctuations in
potassium are intended or anticipated. This
assessment is usually combined with biochemical
measurement, to define abnormalities and to
monitor therapy. Measurement of serum or
plasma potassium is the best biochemical index
of potassium status, despite the fact that this
measurement represents less than 2% of total
body content.
A.naesthesia and Intensive Care, Vol. V, No. 4, November, 1977
 POTASSIUM METABOLISM
Extracellular potassium concentration may
at times deviate acutely in a direction opposite
to the abnormality of total body content, as in
diabetic ketoacidosis. In acute fluctuations of
potassium distribution, such as occur with
disturbances of acid-base balance, it is the
plasma concentration which is the most critical
value, irrespective of total-body balance. An
acute disturbance of plasma level will disturb
transmembrane potential more than a chronic
imbalance, where intra- and extracellular,
concentrations tend to change in the same
direction (Seldin, Carter and Rector 1971).
Because acute manipUlation of plasma potassium
is potentially lethal, it is critical to be aware of
artifacts which give spurious potassium measure-
ments (Table 2) and to avoid acute treatment
on the basis of a single, unexpected laboratory
result.
Measurement of total body potassium is
more complex, requiring either a whole-body
counter (4°K) or administration of isotope (12K).
Such measurements may confuse rather than
improve assessment, because of illness-related
changes in body composition which produce
secondary loss of potassium. The potassium
content of adipose tissue is low, so that a
disproportionate decrease in muscle mass will
give low total potassium without a true deficiency
(de Deuxchaisnes and Mach 1974). This
measurement is most useful in overall assessment
of body composition, or in serial studies of the
same subject, but has very limited routine
application. Results must always be interpreted
cautiously in chronically ill patients because
replacement of a non-deficiency creates the
danger of potassium overload.
Measurement of red cell, leukocyte, or
muscle potassium concentrations (Patrick et al.
1972) can suffer from artifacts of sample
preparation and have not found wide use.
Measurement of urinary potassium (without
supplements or diuretics) can be used to
establish urinary loss as the cause of hypoka-
laemia (Kaplan 1967), but considerable faecal
excretion makes this measurement less useful
than urinary sodium measurement.
HYPOKALAEMIA
A low plasma potassium should be suspected
in any patient who has been receiving diuretics
for cardiac failure, cirrhosis with ascites, or
nephrotic syndrome. In each of these situations,
a low effective plasma volume is the rule,
leading to secondary hyperaldosteronism and
chronic potassium loss, which may not be
Anaesthesia and Intensive Care, Vol. V, No. 4, November, 1977
321
adequately covered by routine supplements.
Diuretic treatment of uncomplicated essential
hypertension, on the other hand, is usually
not associated with potassium deficiency
(Wilkinson et al. 1975). Severe, unsuspected
hypokalaemia may follow diuretic or purgative
abuse, or occult vomiting in patients who are
otherwise physically well. Potassium depletion
is seen at its most severe in patients with
chronic, high gastrointestinal obstruction, where
TABLE 1
Hypokalaemia
Gastrointestinal
Vomiting or Gastric Aspiration.
Malabsorptior:.
Diarrhoea.
Laxative Abuse.
Ureterosigmoidostomy.
Fistulae.
Mineralocorticoid Excess
Hypertensive:
Accelerated Hypertension.
Primary Aldosteronism.
Essential Hypertension plus Diuretics.
Cushing's Syndrome.
Ectopic ACTH Syndrome.
Licorice, Carbenoxolone
Normotensive:
Treated Heart Failure.
Nephrotic Syndrome.
Cirrhosis, Liver Failure.
Diuretic Abuse.
Bartter's Syndrome.
Renal Tubular Acidosis
Other
Alkalosis: Metabolic, Respiratory.
Insulin-Induced Hypoglycaemia.
Periodic Paralysis:
Familial, Thyrotoxic.
Cardiopulmonary Bypass.
Overhydration : Inappropriate ADH Syndrome.
Low Potassium Diet in Adapted Person.
Acute Renal Failure: Diuretic Phase.
Amphotericin, Carbenicillin.
the major potassium loss is urinary, because of
severe uncompensated metabolic alkalosis. In
most conditions, the potassium aberration is
secondary to another process, but in the hypo-
and hyperkalaemic forms of periodic paralysis,
acute shift of potassium across cell membranes
appears to be the primary abnormality (Zierler
1973). The common causes of hypokalaemia
are outlined in Table 1.
Hypokalaemia, whether found by measure-
ment in a suspect patient, or because of
unexpected arrhythmia, cardiographic change
or delayed return of spontaneous respiration
after anaesthesia, requires acute and chronic
322 J. R. STOCKIGT
management. Intravenous administration of include prior treatment with diuretics, respira-
potassium is the most direct way of repairing tory alkalosis (i\larcial et al. 1969) and hypo-
an acute deficit, but because of the small thermia (H.ittenhouse et al. IH74).
extracellular pool, intravenous administration
must net'er exceed a critical rate of about HYPEI~KALAE:\IIA
20 mmol per hour, no matter how severe the Severc hyperkalacmia, thc major causes of
deficit. Even this rate may be excessive in which arc summarized in Table~, is an important
situations where there is illlpaired potassium medical emergency which may require correction
entry into cells, such as in respiratory acidosis within minutcs. Augmentation of renal excre-
(Scrilmer, Fremont-Smith and Burnell 11.)55). tion is unsatisfactory as a short-term treatment
Because of the layering effect in flexible con- for hyperkalaemia because the onset of action
tainers, serious acute overload can occur if of mineralocorticoicls, such ,L'> deox\'Corticost-
hypertonic additive is not thoroughly mixed erone or H Q(-fluorohydrocortisone, o~curs only
(vVilliams Hl7:)). Peripheral infusion of concen-
TABLE 2
trated poi<L';sium usually causes intense local
pain, which may identify this mistake promptly Hy pcrkalaemia
in a conscious patient.
SpUI-io1tS
In many acute situations, associated I-[aemol ysis.
alterations . in fluid and acid-base halance, Thrombocytosis.
blood sugar and renal function make the Gross Lcukoc\'tosis.
effect of any manipulation of potassium difficult l\r \lsde Exercise during \' cnous Congestion
to predict. Repeated measurement is there- Renal hlsujficiellcy
Acute Eenal Failure.
fore essential to achieve any certainty of result. Sc\'ere Chronic ]{enal Failure.
In almost all potassium-deficient states (except Sodium DeplctioI1.
for renal tubular acidosis and ureterosigmoido- Steroid Deficiency
Addison's Disease.
stomy') there is associated metaholic alkalosis, Isolated Hypoaldosteronism.
which makes repair of the potassium deficit Release from Cells
almost impossible without chloride repletion. Acidosis.
Hence, the importance of KCI ratht'J' than l\Iusc1e Injury.
alkaline potassium (Kassirer et al. l!W:i). In Succinylcholine.
Lcukacmia Chemotherapy.
states of fixed mineralocorticoid excess, such H Y]lerkalacmic Periodic Paralysis.
as primary aldosteronism, sodiulll restrictioll is Ialrogclzic
the key to achieving potassiulll replacement. Hapid Intr,,,,cllous Load.
The fa(:tor:-;, other than supplements, which are Excessive Oral Load.
Impaired Excretioll :
critical in achieving long-term repletion have Sl)ironolactunc.
recently heen re\'iewed (Stockigt 1H77). TriamtereI1c.
Chronic potassium deficiency is usually Amiloric\c.
managed hy' long-term oral supplements, but .-~.------- .. ~~~~- ----
there is no\\' e\'idence that their indiscriminate after a latent period of several hours, and
use i:-; hazardous, especially if there is unrecog- because rcnal function may be unccrtain.
nized renal impairment (Lawson 1H7-!). Short-term correction of lryp(~rkalaemia is best
Plasma potassiulll has been reported to achieved bv increasing cell-entrv of potassium
decrease foIlO\\'ing induction of anaesthesia with either alkali or glucose, but a hyperkalaemic
using Thiopentone, ~itrous oxide and Hal()thanc emergency can also be managed b\' infusion of
(List IH(7). This effect is usually small, but calcium, which antagonizes the cardiotoxic
serious hypokalaemia occurs during canliopul- effects of potassium excess. Before such treat-
ll10nary bqlass. Its mechanism is complcx mcnt is begun, it is vital to rule out artifacts such
and has not been fulh' explained, although thc as haemolysis, thromboC\·tosis (Hartmann,
fall in plasrn~t potassium is clearly' tIle result Audi tore and J ac kson J !);is) , massive leuko-
ot internal redistribution rather than urinarv cytosis (l{ingelhann, Laszlo and Vajda IH74)
excretion (:\Iarcial et al. J !)()!I). The insuliil and forearm exercise during venous occlusion
response to glucose-containing priming fluids (Brown et al. 1(70), which may cause spurious
has been suggested as it cause, although \',tlentin hyperkalaemia.
and Rasmussen (l!n;i) were unable to confirm Correction of systcmic acidosis with
this. Other possible causes for hypokalaemia intravenous bicarbonate is thc fastest, safest,

Anaesthesia alld Intellsive Care, Vol. V, No. 4, November, 1977

 POTASSIUM METABOLISM 323

and most reliable way of correcting hyper- fasiculation and indicate that hyperkalaemia
kalaemia. Furthermore, the recent studies of can be avoided by prior curarization.
Fraley and Adler (1976) indicate that bicarbonate As in the management of hypokalaemia,
may alter transcellular potassium distribution, frequent biochemical follow-up is essential to
irrespective of changes in blood pH and suggest monitor the effects of therapy. Each manoeuvre
that bicarbonate is useful therapy for hyper- used to manipUlate plasma potassium carries
kalaemia, even at compensated blood pH. a risk of overshoot which may be worse than
Glucose loads have also been used to rapidly the original problem. Furthermore, patients
lower plasma potassium, usually with concurrent with potassium imbalance rarely have this as
infusion of insulin, although the latter is their sole abnormality, so that therapy may
dangerous until adrenal insufficiency is ruled have to be modified because of associated
out, and is probably unnecessary in non-diabetics. diseases.
Attempts to restore renal function by repair
ACKNOWLEDGEMENT
of volume deficit and treatment of associated
sepsis are further urgent priorities. The Editor, Australian and New Zealand
In some situations, such as extensive muscle Journal of Medicine, kindly gave permission for
damage, plasma potassium may rise at a rate publication of Figures 1-4.
in excess of the capacity for either excretion
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 POTASSIUM METABOLISM 325

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