Chapter 26
Fluid, Electrolyte, and Acid-Base Balance
1003
26
the body is normal. In the absence of aldosterone, hyperkalemia
is swiF and lethal regardless of K
1
intake (Table 26.1). Conversely,
when a person has an adrenocortical tumor that pumps out tre-
mendous amounts of aldosterone, EC± potassium levels fall so
low that neurons all over the body hyperpolarize and paralysis
occurs.
Regulation of Calcium
and Phosphate Balance
About 99% of the body’s calcium is found in bones in the form
of calcium phosphate salts, which make the skeleton rigid and
strong. ²e bony skeleton provides a dynamic reservoir from
which calcium and phosphate can be withdrawn or deposited to
maintain the balance of these electrolytes in the EC±.
Homeostatic Imbalance
26.4
Ionic calcium in the EC± is important for normal blood clot-
ting, cell membrane permeability, and secretory behavior, but
its most important effect by far is on neuromuscular excitability.
Hypocalcemia increases excitability and causes muscle tetany.
Hypercalcemia is equally dangerous because it inhibits neu-
rons and muscle cells and may cause life-threatening cardiac
arrhythmias (Table 26.1).
EC± calcium ion levels are closely regulated by
parathyroid
hormone (PTH)
, and rarely deviate from normal limits. (²e
hormone calcitonin, produced by the thyroid, is oFen thought
of as a calcium-lowering hormone, but, as we discussed in
Chapter 16, its effects on blood calcium levels in humans are
negligible.) Parathyroid hormone is released by the tiny para-
thyroid glands located on the posterior aspect of the thyroid
gland in the neck. Declining plasma levels of Ca
2
1
directly stim-
ulate the parathyroid glands to release PTH, which promotes an
increase in calcium levels by targeting the following organs (see
also ±igure 16.13 on p. 611):
Bones.
PTH activates bone-digesting osteoclasts, which
break down the bone matrix, releasing Ca
2
1
and HPO
4
2
2
to
the blood.
Kidneys.
PTH increases Ca
2
1
reabsorption by the renal tu-
bules while decreasing phosphate ion reabsorption. In this
way, calcium conservation and phosphate excretion go hand
in hand. ²e
mathematical product
of Ca
2
1
and HPO
4
2
2
con-
centrations ([Ca
2
1
]
3
[HPO
4
2
2
]) in the EC± remains con-
stant, preventing calcium-salt deposits in bones or soF body
tissues.
Small intestine.
PTH enhances intestinal absorption of Ca
2
1
indirectly by stimulating the kidneys to transform vitamin D
to its active form, which is necessary for the small intestine to
absorb Ca
2
1
.
Most Ca
2
1
is reabsorbed passively in the PCT via diffusion
through the paracellular route (a process driven by its electro-
chemical gradient). However, as with other ions, Ca
2
1
reab-
sorption is fine-tuned in the distal nephron. PTH-regulated
Ca
2
1
channels control Ca
2
1
entry into DCT cells at the apical
loop absorbs another 10–20% or so regardless of need, leaving
about 10% at the beginning of the collecting ducts. ²e respon-
sibility for K
1
balance falls chiefly on the collecting ducts. ²ey
achieve this balance mainly by changing the amount of K
1
se-
creted
into the filtrate.
As a rule, K
1
levels in the EC± are sufficiently high that K
1
needs to be excreted, and the principal cells of the cortical col-
lecting ducts secrete K
1
into the filtrate. (At times, the amount
of K
1
excreted may actually exceed the amount filtered.) When
EC± potassium concentrations are abnormally low, the renal
principal cells conserve K
1
by reducing its secretion and excre-
tion to a minimum. Note that these principal cells are the same
cells that mediate aldosterone-induced reabsorption of Na
1
and
ADH-stimulated reabsorption of water.
Additionally,
type A intercalated cells
, a unique population
of collecting duct cells, can reabsorb some of the K
1
leF in the
filtrate (in conjunction with active secretion of H
1
), thereby
helping to reestablish K
1
(and pH) balance. However, keep in
mind that the main thrust of renal regulation of K
1
is to
excrete
it. Because the kidneys have a limited ability to retain K
1
, it may
be lost in urine even in the face of a deficiency. Consequently,
people who don’t eat potassium-rich foods can eventually de-
velop a severe deficiency.
Influence of Plasma Potassium Concentration
²e single most important factor influencing K
1
secretion is the
K
1
concentration in the EC±. A high-potassium diet increases
the K
1
content of the EC±. ²is favors entry of K
1
into the prin-
cipal cells of the cortical collecting duct and prompts them to
secrete K
1
into the filtrate so that more of it is excreted. Con-
versely, a low-potassium diet or accelerated K
1
loss depresses
its secretion (and promotes its limited reabsorption) by the col-
lecting ducts.
Influence of Aldosterone
²e second factor influencing K
1
secretion into the filtrate is al-
dosterone. As it stimulates the principal cells to reabsorb Na
1
, al-
dosterone simultaneously enhances K
1
secretion (see ±igure 26.8).
Adrenal cortical cells are
directly
sensitive to the K
1
content of the
EC± bathing them. When it increases even slightly, the adrenal cor-
tex is strongly stimulated to release aldosterone, which increases
K
1
secretion by the exchange process we just described. ²e result
is that K
1
controls its own concentrations in the EC± via feedback
regulation of aldosterone release.
Aldosterone is also secreted in response to the renin-
angiotensin-aldosterone mechanism previously described.
Given the opposing effects of aldosterone on plasma Na
1
and
K
1
, you might expect that Na
1
- and volume-driven changes in
aldosterone would disrupt K
1
balance. ²is generally does not
occur because other compensatory mechanisms in the kidneys
maintain plasma K
1
.
Homeostatic Imbalance
26.3
To reduce their NaCl intake, many people have turned to salt sub-
stitutes, which are high in potassium. However, heavy consump-
tion of these substitutes is safe only when aldosterone release in
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