818
UNIT FIVE
causes the kidneys to conserve calcium ions (through
increased tubular reabsorption) and increases the urinary
excretion of phosphate ions. The increased phosphate excre-
tion offsets the increased plasma phosphate. Thus, the net
effect of the hormone is to return the
calcium ion
concentra-
tion of the extracellular fl
uid to normal levels but to maintain
a normal
phosphate ion
concentration
(f
g. 21.8)
.
Abnormal increases in blood calcium (hypercalcemia) sometimes
result from hyperparathyroidism, in which excess secretion of PTH
increases bone resorption. Hypercalcemia may also be caused by
cancers, particularly those originating in the bone marrow, breasts,
lungs, or prostate gland. Usually the increase in calcium occurs when
cancer causes bone tissue to release ions. In other cases, however,
the blood calcium concentration increases when cancer cells produce
biochemicals that have physiological eF
ects similar to parathyroid hor-
mone. This most often happens in lung cancer. Symptoms of cancer-
induced hypercalcemia include weakness and fatigue, impaired mental
function, headache, nausea, increased urine volume (polyuria), and
increased thirst (polydipsia).
Abnormal decreases in blood calcium (hypocalcemia) may result
from reduced availability of PTH following removal of the parathy-
roid glands, or from vitamin D deficiency, which may result from
decreased absorption following gastrointestinal surgery or excess
excretion due to kidney disease. Hypocalcemia may be life threaten-
ing if it causes muscle spasms in the airways and cardiac arrhythmias.
Administering calcium salts and high doses of vitamin D to promote
calcium absorption can correct this condition.
Generally, the regulatory mechanisms that control posi-
tively charged ions secondarily control the concentrations
of negatively charged ions. For example, chloride ions (Cl
),
the most abundant negatively charged ions in the extracellu-
lar fl
uids, are passively reabsorbed from the renal tubules in
response to the active reabsorption of sodium ions. That is,
the negatively charged chloride ions are electrically attracted
to the positively charged sodium ions and accompany them
as they are reabsorbed.
Some negatively charged ions, such as phosphate ions
(PO
4
–3
) and sulfate ions (SO
4
–2
), also are partially regulated
by active transport mechanisms that have limited transport
capacities. Thus, if the extracellular phosphate ion concen-
tration is low, the phosphate ions in the renal tubules are
conserved. On the other hand, if the renal plasma thresh-
old is exceeded, the excess phosphate will be excreted in the
urine. Clinical Application 21.2 discusses symptoms associ-
ated with sodium and potassium imbalances.
PRACTICE
17
How does aldosterone regulate sodium and potassium ion
concentration?
18
How is calcium regulated?
19
What mechanism regulates the concentrations of most negatively
charged ions?
Regulation of Electrolyte Output
The concentrations of positively charged ions, such as
sodium (Na
+
), potassium (K
+
), and calcium (Ca
+2
), are par-
ticularly important. Certain concentrations of these ions are
vital for nerve impulse conduction, muscle ±
ber contraction,
and maintenance of cell membrane permeability. Potassium
is especially important in maintaining the resting potential
of nerve and cardiac muscle cells, and abnormal potassium
levels may disrupt the functioning of these cells.
Sodium ions
account for nearly 90% of the positively
charged ions in extracellular fl
uids. The kidneys and the hor-
mone aldosterone primarily regulate these ions. Aldosterone,
which the adrenal cortex secretes, increases sodium ion
reabsorption in the distal convoluted tubules and collect-
ing ducts of the nephrons. A decrease in sodium ion con-
centration in the extracellular fl
uid stimulates aldosterone
secretion via the renin-angiotensin system, as described in
chapter 20 (p. 790 and ± g. 20.20).
Aldosterone also regulates
potassium ions.
An important
stimulus for aldosterone secretion is a rising potassium ion
concentration, which directly stimulates cells of the adrenal
cortex. This hormone enhances the renal tubular reabsorp-
tion of sodium ions and, at the same time, stimulates renal
tubular secretion of potassium ions
(f
g. 21.7)
.
Recall from chapter 13 (p. 502) that the calcium ion
concentration dropping below normal directly stimulates
the parathyroid glands to secrete parathyroid hormone.
Parathyroid hormone increases activity in bone-resorbing
cells (osteoclasts), which increases the concentrations of
both calcium and phosphate ions in the extracellular flu-
ids. Parathyroid hormone also indirectly stimulates calcium
absorption from the intestine. Concurrently, this hormone
Renal tubules
increase reabsorption of
sodium ions and increase
secretion of potassium ions
Aldosterone is secreted
Adrenal cortex is signaled
Potassium ion
concentration increases
Sodium ions are
conserved and potassium
ions are excreted
FIGURE 21.7
If the potassium ion concentration increases, the
kidneys conserve sodium ions and excrete potassium ions.
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