Chapter 26
Fluid, Electrolyte, and Acid-Base Balance
water simply flows on by. Te result is dilute urine and a re-
duced volume of body fluids. When ADH levels are high, aq-
uaporins are inserted in the principal cell apical membranes,
nearly all of the filtered water is reabsorbed, and a small volume
of concentrated urine is excreted.
Osmoreceptors of the hypothalamus sense the ECF solute
concentration and trigger or inhibit ADH release from the pos-
terior pituitary accordingly
(Figure 26.6)
. An increase in ECF
osmolality prompts ADH release by stimulating the hypotha-
lamic osmoreceptors. In contrast, a decrease in ECF osmolality
inhibits ADH release and allows more water to be excreted in
urine, restoring normal blood osmolality.
Large changes in blood volume or blood pressure also influ-
ence ADH secretion. A decrease in blood pressure increases
ADH release both directly via baroreceptors in the atria and
various blood vessels, and indirectly via the renin-angiotensin-
aldosterone mechanism.
Te key word here is “large” because changes in ECF osmolality
are much more important as day-to-day stimulatory or inhibitory
factors. Factors that trigger ADH release by reducing blood volume
include excessive sweating, vomiting, or diarrhea; severe blood loss;
traumatic burns; and prolonged fever. Under these conditions, high
concentrations of ADH also act to constrict arterioles, directly in-
creasing blood pressure—hence its other name:
. For a
summary of how renal mechanisms involving ADH, aldosterone,
and angiotensin II tie into overall controls of blood volume and
blood pressure, see Figure 26.10 (p. 1002), but remember that the
main thrust of ADH is to maintain ECF osmolality.
Disorders of Water Balance
Few people really appreciate the importance of water in keeping
the body’s “machinery” working at peak efficiency. Te principal
abnormalities of water balance are dehydration, hypotonic hy-
dration, and edema—each presenting a special set of problems.
is defined as fluid loss, either the loss
of water or the loss of water and solutes together. For example,
when water output exceeds intake over a period of time, the
body becomes dehydrated. Dehydration is a common sequel
to hemorrhage, severe burns, prolonged vomiting or diarrhea,
profuse sweating, water deprivation, and diuretic abuse. Dehy-
dration may also be caused by endocrine disturbances, such as
diabetes mellitus or diabetes insipidus (see Chapter 16).
Early signs and symptoms of dehydration include a “cottony”
or sticky oral mucosa, thirst, dry flushed skin, and decreased
urine output (
). Prolonged dehydration may lead to
weight loss, fever, and mental confusion. Another serious con-
sequence of water loss from plasma is inadequate blood volume
to maintain normal circulation and ensuing
hypovolemic shock
Water and solutes can be lost together (as in hemorrhage), or
more water than solutes can be lost (as in profuse sweating). If
the body loses more water than solutes, water moves osmotically
rhage) also triggers the thirst mechanism. Tese changes in
volume or pressure are signaled by baroreceptors that directly
activate the thirst center, and by angiotensin II as we described
in Chapter 19.
Collectively, these events cause a subjective sensation of
thirst, which motivates us to get a drink. Tis mechanism ex-
plains why some cocktail lounges provide free
snacks to
their patrons.
Curiously, thirst is quenched almost as soon as we begin
drinking water, even though the water has yet to be absorbed
into the blood. How does this happen? Incoming liquid mois-
tens the mucosa of the mouth and throat and activates osmore-
ceptors and stretch receptors in the stomach and small intestine,
providing feedback signals that inhibit the thirst center. Prema-
ture quenching of thirst prevents us from drinking more than
we need and overdiluting our body fluids, and allows time for
the osmotic changes to come into play as regulatory factors.
As effective as thirst is, it is not always a reliable indicator
of need. Tis is particularly true during athletic events, when
thirst can be satisfied long before sufficient liquids have been
drunk to maintain the body in top form. Additionally, elderly
or confused people may not recognize or heed thirst signals.
In contrast, fluid-overloaded renal or cardiac patients may feel
thirsty despite their condition.
Regulation of Water Output
Output of certain amounts of water is unavoidable. Such
tory water losses
help to explain why we cannot survive for long
without drinking. Even the most heroic conservation efforts by
the kidneys cannot compensate for zero water intake. Obligatory
water loss includes the
insensible water losses
described above,
water that accompanies undigested food residues in feces, and a
minimum daily
sensible water loss
of 500 ml in urine.
Obligatory water loss in urine reflects the fact that human
kidneys must normally flush 600 mmol per day of urine sol-
utes (end products of metabolism and so forth) out of the body
in water. Te maximum concentration of urine is about 1200
mOsm, so at least 500 ml of water must be excreted.
Beyond obligatory water loss, the solute concentration and vol-
ume of urine excreted depend on fluid intake, diet, and water loss
via other avenues. For example, if you perspire profusely on a hot
day, you have to excrete much less urine than usual to maintain
water balance. Normally, the kidneys begin to eliminate excess wa-
ter about 30 minutes a±er it is ingested. Tis delay reflects the time
required to inhibit ADH release. Diuresis reaches a peak about 1
hour a±er drinking and declines to its lowest level a±er 3 hours.
Influence of Antidiuretic Hormone (ADH)
Te amount of water reabsorbed in the renal collecting ducts is
proportional to ADH release. When ADH levels are low, most
of the water reaching the collecting ducts is not reabsorbed be-
cause the lack of aquaporins in the apical membranes of the
principal cells prevents the movement of water. Instead, the
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