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OCR for page 378
Potas slum
Potassium (K), a light metal, makes up 2.6 percent of the earth's crust.
It is found mainly within the cells of the animal body and is a dietary
essential for all animals.
It is widely distributed in feed sources, but the levels are highly
variable. Overt deficiencies are seldom encountered in animals.
Usually, forages are higher in potassium than concentrates. Certain
lush growing forages, such as cereals, may contain high levels of the
element. In these cases, the potassium may interfere with magnesium
utilization. Forages that have been subjected to weathering may con-
tain low levels of the element.
ESSENTIALITY
Animals have a dietary requirement for potassium. Deficiencies have
been produced in cattle, chicks, swine, and other animals. The quanti-
tative requirement varies among species. Apparently, the requirement
is higher for ruminants than nonruminants. For example, the require-
ments are 0.6 to 0.8 percent for cattle (National Research Council,
1976) and 0.20 to 0.39 percent for swine (National Research Council,
19791. Frequently, the feed sources supply sufficient amounts to meet
the dietary requirement. Exceptions are finishing cattle fed high con-
centrate diets, cattle fed high nonprotein nitrogen diets, dairy cattle on
high corn silage feeding programs, and cattle grazing or fed weathered
roughages, i.e., late fall and winter range feeding conditions.
378
OCR for page 379
Potassium
METABOLISM
379
Potassium is absorbed mainly from the upper small intestine, but some
absorption also occurs in the lower small intestine and large intestine
(Church and Pond, 1974~. Absorption from the intestine appears to be
by simple diffusion. The main functions of potassium in the animal are
for osmotic equilibrium, maintenance of acid-base balance, enzyme
reactions for phosphorylation of creatine, pyruvate kinase activity,
cellular uptake of amino acids, carbohydrate metabolism, protein
synthesis, and maintenance of normal heart and kidney tissue (Church
and Pond, 19741.
Excess potassium is usually excreted through the urine. AIdosterone
and sodium intake affect potassium excretion. The hormone increases
sodium reabsorption in the kidney, and there is usually an inverse
relationship between sodium and potassium excretion. Ward (1966b)
reviewed potassium metabolism in ruminants.
SOURCES
Potassium is present in feedstuffs in different amounts. Generally, it is
higher in forages than grains (National Research Council, 1971~. For
example, corn grain contains 0.35 percent potassium, dry basis, com-
pared to 1.64 percent for corn stover. Alfalfa hay frequently contains
over 2 percent potassium. Actively growing wheat pasture forage may
contain 5 percent potassium (Miller, 19391. However, weathered range
grasses may contain as low as 0.1 percent potassium. Generally, sum
plementa] potassium is supplied as potassium bicarbonate, carbonate,
chloride, and sulfate.
TOXICOSIS
Potassium toxicosis is not likely to occur under practical situations.
However, since high dietary levels of potassium interfere with magne-
sium absorption in ruminants, ingestion of such levels may predispose
the animals to hypomagnesemic tetany (Newton et al., 1972~. Toxicosis
may occur from feeding excess levels of potassium supplements.
LOW LEVELS
Increasing the level of dietary potassium from 0.7 to 3.0 percent linearly
decreased energy and weight gain in lambs (Jackson et al., 19711.
OCR for page 380
380 MINERAL TOLERANCE OF DOMESTIC ANIMALS
Feeding 1 percent potassium chloride (0.5 percent potassium) reduced
the incidence of urinary calculi in lambs (Crookshank, 1966), but had no
effect on the incidence in cattle (Hoar e! al., 19701. Feeding potassium
chloride at 1 or 2 percent (0.5 or 1.0 percent potassium provided some
protection from calculi in lambs when the diet contained 0.5 percent
phosphorus, but was without effect when the diet contained 0.7 percent
phosphorus (Emerick e! al., 1972~. Feeding 1 or 2 percent potassium
acetate (0.4 or 0.8 percent potassium) increased gain and feed efficiency
in swine (Liebho~z et al., 1966~. The 1 percent supplementation level
was more effective than the 2 percent.
HIGH LEVELS
Intravenous administration of 306 mg potassium chloride per kilogram
per dose (160 mg potassium per kilogram) did not cause death in calves,
but administration of 629 mg potassium chloride per kilogram (330 mg
potassium per kilogram) resulted in death (Bergman and Sellers, 1953~.
Severe signs resulted with plasma potassium levels of about 31.3 mg/d1,
and the only death was in an animal in which potassium reached 50
mg/dl gradually over a period of 168 minutes. When plasma potassium
reached 31 mg/d1, the heart rate became slower (Bergman and Sellers,
1954~. Respiratory movements increased in rate and amplitude in all
potassium experiments. Atrial flutter and complete atrioventricular
block with nodal rhythm was observed in two of eight experiments.
Administration of 393 g potassium as potassium chloride by stomach
tube to cows weighing about 300 kg resulted in one death, two cattle
requiring treatment, and two showing no toxic signs (Dennis and Har-
baugh, 1948~. Two animals administered 182 and 240 g potassium
showed no clinical signs, and a third one given 212 g developed milk
fever signs that responded to calcium gluconate treatment. Oral
administration of 501 mg potassium per kilogram as potassium chloride
to a 475-kg dairy cow by stomach tube resulted in death within 10
minutes, apparently from cardiac arrest (Ward, 1966a). The author
pointed out that this dose represented about one-half the daily intake of
similar cows that were fed 15 kg alfalfa hay per day, and that apparently
did not suffer ill effects.
The recognition that incidence of grass tetany seemed to be higher
in animals grazing pastures that had been fertilized with potassium
(Dryerre, 1932) stimulated interest in the role of potassium in the dis-
turbance. Increasing the potassium level in a liquid diet from 1.2 to 5.8
OCR for page 381
Potassium
381
percent, dry basis, resulted in death of three of eight calves (Blaxter et
al., 19601. The clinical signs before death were cardiac insufficiency,
edema, severe muscular weakness, and muscular atony. No abnor-
malities in magnesium metabolism were observed.
Administration of a combination of 157 g potassium chloride and
157 g of trans-aconitic acid or citric acid per 100 kg of body weight
resulted in a high incidence of tetany resembling field cases of grass
tetany in 237-kg yearling cattle (Bohman et al., 1969~. It appeared that
the combinations were required for the effects. Plasma magnesium was
not affected by the treatments. Acute toxicosis was produced by oral
administration of 500 g potassium chloride and 500 g citric acid to
440-kg fistulated steers (Rumsey and Putnam, 1972~. Death was pre-
ceded by darkening of the blood, frequent urination, frequent attempts
to defecate, intense muscular tremors, protruding eyes, and loss of
ability to stand. Struggling was noted after the steers were unable to
stand. Rapid changes in EKG patterns were noted, and respiration rate
was increased.
Plasma levels of potassium and immunoreactive insulin were ele-
vated by intravenous infusion of 5l, 64, and 135 mg potassium per
kilogram as potassium chloride in calves and intraruminal infusion of
4~0 mg potassium per kilogram in cows (Lentz et al., 19761. Admin-
istering of 64 mg potassium per kilogram resulted in lower plasma
potassium and higher plasma glucose and insulin in magnesium def~-
cient calves than in normal calves.
Feeding a diet with approximately ~ percent potassium to ewes did
not affect blood serum levels of magnesium, calcium, or potassium
(Pearson e! al., 1949~. Later, including 5 percent potassium as bicar-
bonate in a ewe diet lowered serum magnesium, but did not produce
clinical signs (Kunkel et al., 1953~. Feeding a high-potassium hay or
supplemental potassium increased serum potassium, but was without
effect on serum magnesium in sheep (Eaton and Avampato, 19531.
Apparent absorption of magnesium in sheep was severely reduced by
feeding a diet containing about 34 percent crude protein and 4.7 percent
potassium, dry basis (Fontenot e! al., 1960~.
Feeding a diet with approximately 4 percent potassium depressed
magnesium absorption by about 30 percent in sheep (House and Van
Campen, 1971~. Magnesium absorption in sheep was reduced 46 per-
cent when the potassium level of the diet was raised from 0.7 to S.5
percent, dry basis (Newton et al., 1972~. Feeding a high potassium level
resulted in similar increases in fecal magnesium, expressed as grams,
but not as percent of intake over a wide range of dietary magnesium
OCR for page 382
382 MINERAL TOLERANCE OF DOMESTIC ANIMALS
intakes (Frye, 1975~. Feeding a diet containing 4 percent potassium
resulted in a faster disposal of intravenously administered magnesium,
compared to feeding 0.9 percent potassium (House and Bird, 19751.
Single intraperitoneal injections of 0.575 g potassium chloride per
kilogram (~.302 g potassium per kilogram) of body weight were fatal to
rabbits within 1~30 minutes, with terminal plasma potassium of 58 to
85 mg/dl (Truscoe and Zwemer, 1953~.
Including 0.5 to 4.5 g potassium in the diet of adrenalectomized dogs
resulted in potassium toxicosis (Allerset al., 19361. The signs of adrenal
insufficiency were accompanied by a high level of potassium in the cells
(Wilson, 1937~. Recovery could be accomplished either by administra-
tion of sodium chloride or adrenal cortical extract. Potassium admin-
istered by intravenous injection was distributed in a volume greater
than that of the extracellular fluid of dogs (Winkler and Smith, 19381.
This indicates that it enters some and probably most cells in the body.
Death occurred in dogs in which potassium chloride was injected
intravenously when serum potassium reached 47 to 78 mgIdl (Winkler
et al., 19391. The toxic effects seemed to be specific for the heart,
without similar effects on skeletal muscle. Injecting toxic levels of
potassium in dogs resulted in intraventricular block and diastolic arrest
(Winkleret al., 1940~.
Infusion of a high-potassium solution intravenously prevented induc-
tion of atrial fibrillation by acetylcholine or vagal stimulation in dogs
(Hashimoto et at., 1970~. Dogs exhibited electrocardiographic evidence
of prelethal cardiotoxicosis in about 3 hours from infusing 78 mg potas-
sium chloride per kilogram (41 mg potassium per kilogram) of body
weight (Hiatt et al., 1975~. At that time serum potassium level was
40 41 mg/dl.
Adaptation to high levels of potassium occurred in the rat by gradu-
ally increasing the size of the dose (Thatcher and Radike, 1947~. Ad-
ministration of adrenal extract to the rats was helpful in resisting the
potassium ion, but the effect was not as beneficial as potassium
adaptation.
Feeding a diet with 5 percent potassium as the bicarbonate or 3
percent as the carbonate resulted in similar marked depressions in
growth rate of rats (Pearson, 19481. High mortality was observed from
feeding the 5 percent potassium diet supplied as carbonate. Increasing
dietary magnesium reduced mortality. Feeding a high-potassium (2.9
percent) diet depressed growth in rats (Colby and Frye, 1951~. When
combined with a high-calcium level (2.5 percent of diet), increased
mortality and lowered blood magnesium were noted.
One half of the rats that consumed the 1.04 g of potassium per 100 g
OCR for page 383
Potassium
3X3
of body weight per day died with signs of potassium toxicosis (Drescher
et al., 1958~. It was concluded that excess dietary potassium produces
widening of the zone giomerulosa of the adrenal cortex in rats (Hartroft
and Sowa, 1964~. High dietary potassium (3.60 g potassium per 100 g
feed) decreased plasma renin level (Sealey et al., 1970~.
Feeding a diet with 0.68 g potassium per 100 g for several weeks
resulted in magnesium depletion in rats (Duarte, 1974~. Duarte sug-
gested that the effect may have been due to an enhanced aldosterone
secretion or competition for transport between magnesium and potas-
sium. A 200 percent increase in density of cristae mitochondriales in
proximal and distal tubules of kidney cortex was observed in rats fed
7.82 mg of potassium per 100 g of diet for 6 weeks (Pfaller et al., 19741.
Similar effects were produced by aldosterone injection.
The LD50 (~10 minutes) for immature mice weighing ~11 g was
reported to be 66.5 me potassium chloride (34.9 mg potassium) per 100
g of body weight and 57.5 mg (30.2 mg), injected intraperitoneally for
adrenalectomized mice (Truszkowski and Duszynska, 1940~. Resis-
tance of adrenalectomized mice could be raised above that for normal
mice by injections of adrenal extract.
FACTORS INFLUENCING TOXICITY
The deleterious effect of high dietary potassium on magnesium utiliza-
tion by ruminants is well documented (Fontenotet al., 1973~. However,
it appears that a high-magnesium level may offer some protection
against potassium toxicity. Increasing the magnesium content of a diet
containing 5 percent potassium as carbonate reduced mortality in rats
(Pearson, 19481. Acute magnesium loading of potassium adapted rats
caused an increase in urinary potassium excretion (Duarte, 19741.
Adaptation to the potassium ion increases the tolerance of the albino rat
to potassium toxicity (Thatcher and Radike, 1947; Drescher et al.,
19581. Administration of adrenal extract resulted in increased resis-
tance in rats (Thatcher and Radike, 1947) and mice (Truszkowski and
Duszynska, 1940~.
Sodium salts, at least under some conditions, reduce effects of high
dietary potassium. Recovery of adrenalectomized dogs showing signs
of adrenal insufficiency caused by high-potassium intake can be pro-
duced by administration of sodium salts (Nilson, 1937~. Drops in serum
potassium level in dogs of 34 to 53 percent resulted from parenteral
administration of magnesium sulfate, indicating the relationship of
these elements (Smith, 1949~.
OCR for page 384
384 MINERAL TOLERANCE OF DOMESTIC ANIMALS
TISSUE LEVELS
Feeding a 5 percent potassium diet resulted in higher potassium levels
in skeletal muscle, heart muscle, kidney, and thymus of rats (Meyer et
al., 1950), compared to rats fed 0.005 percent potassium. The difference
indicated, at least partly, an effect of potassium deficiency. Compared
to feeding a 0.50 percent potassium diet, tissue levels were not
substantially elevated by feeding 5 percent potassium. No differences
occurred in potassium in carcass or heart muscle in rats fed levels
ranging from 0.06 to 1.5 mg potassium per 100 g of body weight
(Drescher et al., 19581.
MAXIMUM TOLERABLE LEVELS
No overt signs were produced in ruminants by oral administration of
potassium at levels of 3 percent or lower, unless high levels of citric or
trans-aconitic acid were administered also. Alfalfa hay, a recognized
high-quality roughage, may contain over 2 percent potassium, dry basis
(National Research Council, 1971~. The maximum tolerable level is set
at 3 percent for cattle and sheep. However, a level of 3 percent potas-
sium may lower magnesium. absorption. Data for nonruminants are
limited but a maximum level of 3 percent appears to be satisfactory.
SUMMARY
Potassium, found mainly within the cells of the animal body, performs
essential metabolic functions. Animals have a dietary requirement for
the mineral, which varies with species. It is distributed in feeds, with
forages usually containing higher levels than concentrates.
High levels of dietary potassium are toxic to both ruminant and
nor~ruminant animals. Excessive intake of potassium appears to inter-
fere with the absorption and utilization of magnesium. The heart and
adrenal glands are adversely affected by excessive intake of potas-
sium. The toxicity of potassium can be mitigated by sodium salts and
increased intake of magnesium.
Tissue levels are only slightly affected by dietary potassium levels
above the level required in the diet.
OCR for page 385
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Potassium
REFERENCES
389
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OCR for page 390
390 MINERAL TOLERANCE OF DOMESTIC ANIMALS
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control of renin secretion. J. Clin. Invest. 49:2119.
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Representative terms from entire chapter:
potassium chloride