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CHAPTER 13 SUMMARY
The ECF provides the internal environment in which cells must operate, and its regulation is a key
feature of homeostasis in animals.
•To achieve balance of the ECF, input of water, salts, and other key molecules must equal the
output. Output can be regulated, as in excretory processes, or unregulated, as in water loss via
uncontrolled evaporation.
•Body water is distributed between the intracellular and extracellular fluid compartments.
In vertebrates, the plasma and interstitial fluid are separated by the blood vessel walls, whereas
the ECF and ICF are separated by cellular plasma membranes.
Osmotic and Volume Balance
Basic cell components yield about 300 mOsm of osmotic concentration. Several forces can
threaten cell osmotic homeostasis. Osmosis problems occur if the ECF becomes too concentrated
or too dilute due to (1) evaporation into air, (2) osmosis into or out of the environment (e.g., into
seawater at 1000 mOsm, (3) freezing, (4) physiological functions such as excretion, and (5)
diseases such as diabetes. Organisms have evolved two strategies to cope with osmotic
challenges.
•Osmoconformers use special organic osmolytes in their cells, which elevate osmotic pressure
and which, unlike salts, are compatible with macromolecules. Some osmolytes can counteract
protein-destabilizing stresses such as urea and hydrostatic pressure. Pure osmoconformers (e.g.,
most marine organisms) have ECFs with NaCl concentrations about the same as the environment,
while cells adjust organic osmolytes with any osmotic changes. Hypo-ionic osmoconformers (e.g.,
cartilaginous fishes) have ECFs with NaCl levels less than the environment and with organic
osmolytes in the ECF as well as ICF.
•Osmoregulators rely on special transport mechanisms to maintain internal osmotic constancy.
Hypo-osmotic regulators (e.g., bony fish and higher vertebrates) drink seawater and transport
salt out of their bodies to maintain internal osmolarity of about 300-400 mOsm. Impermeable
epithelia and specialized organs (gills, salt glands, kidneys) regulate this. Hyperosmotic regulation
occurs in freshwater and in terrestrial habitats, again using impermeable epithelia and specialized
organs.
Mammalian Osmoregulation
•In mammals, the essential components of fluid balance are control of ECF volume by
maintaining salt balance and control of ECF osmolarity by maintaining water balance. Change in
ECF volume alters the arterial blood pressure, an additional problem.
•Changes in ECF volume and arterial blood pressure are compensated for in the long run by Na+regulating mechanisms. Salt intake is controlled by salt hunger, and control of salt output in the
urine is closely regulated. Blood-pressure regulating mechanisms can vary the GFR, and
accordingly the amount of Na+ filtered, by adjusting the caliber of the afferent arterioles
supplying the glomeruli. Simultaneously, blood-pressure-regulating mechanisms can vary the
secretion of aldosterone, the hormone that promotes Na + reabsorption by the renal tubules. By
varying Na+ filtration and Na+ reabsorption, the extent of Na+ excretion in the urine can be
adjusted to regulate the plasma volume and subsequently the arterial blood pressure in the long
term.
•Changes in ECF osmolarity are primarily detected and corrected by the systems responsible for
maintaining H2O balance. Regulation of free H2O balance is accomplished largely by vasopressin
and, to a lesser degree, by thirst. Changes in vasopressin secretion and thirst are both governed
primarily by hypothalamic osmoreceptors, which monitor ECF osmolarity. The amount of
vasopressin secreted determines the extent of free H2O reabsorption by the distal portions of the
nephrons, thereby determining the volume of urinary output. Simultaneously, the intensity of
thirst controls the volume of fluid intake. However, because the volume of fluid drunk is often not
directly correlated with the intensity of thirst, control of urinary output by vasopressin is the most
important regulatory mechanism for maintaining H2O balance.
•Long-term control of circulatory functions such as blood pressure involves maintenance of
proper plasma volume through the kidneys’ control of salt and water balance. In hemorrhagic
shock, a variety of cardiovascular, neural and renal mechanisms are triggered to correct for drop
in blood pressure, blood volume and salt.
Acid–Base Balance
Hydrogen-ion concentration frequently is expressed in terms of pH, which is the logarithm of 1/[
H+]. Acids liberate free hydrogen ions (H+) into solution; bases bind with free hydrogen ions and
remove them from solution.
•The normal pH of mammalian plasma is 7.4, slightly alkaline compared to neutral H 2O, which
has a pH of 7.0.
•Fluctuations in H+ ion have profound effects, most notably: (1) changes in neuromuscular
excitability, with acidosis depressing excitability, especially in the central nervous system, and
alkalosis producing overexcitability of both the peripheral and the central nervous systems; (2)
disruption of normal metabolic reactions by altering the structure and function of all enzymes;
and (3) alterations in plasma [K+] brought about by H+- induced changes in the rate of K+
elimination by the kidneys.
•Acid–base balance refers to the regulation of H+ concentration ([H+]) in the body fluids. To
precisely maintain [H+], input of H+ by means of metabolic production of acids within the body
must continually be matched with H+ output by urinary excretion of H+ and respiratory removal
of H+-generating CO2.
•Furthermore, between the time of this generation and elimination, H + must be buffered within
the body to prevent marked fluctuations in [H +]. A pH lower than normal (higher [H+] than
normal) is indicative of a state of acidosis. A pH higher than normal (lower [H +] than normal)
characterizes a state of alkalosis. In vertebrates, the three lines of defense for resisting changes
in [H+]are as follows:
•Chemical buffer systems, the first line of defense, each consist of a pair of chemicals involved in
a reversible reaction, one that can liberate H+ and the other that can bind H+. A buffer pair acts
immediately to minimize any changes in pH that occurs by acting according to the law of mass
action.
•The respiratory system in air breathers, constituting the second line of defense, normally
eliminates the metabolically produced CO 2 so that H2CO3 does not accumulate in the body fluids.
When the chemical buffers alone have been unable to immediately minimize a pH change, the
respiratory system responds within a few minutes by altering its rate of CO 2 removal. An increase
in [H+] arising from non-carbonic-acid sources stimulates respiration so that more H2CO3-forming
CO2 is blown off, compensating for the acidosis by reducing the generation of H+ from H2CO3.
Conversely, a fall in [H+] depresses respiratory activity so that CO2 and thus H +-generating
H2CO3 can accumulate in the body fluids to compensate for the alkalosis.
•The kidneys are the third and most powerful line of defense. They require hours to days to
compensate for a deviation in body fluid pH. However, they not only eliminate the normal
amount of H+ produced from non-H2CO3 sources, but they can also alter their rate of H +
removal in response to changes in both non- HCO3- and H2CO3 acids. In contrast, the lungs can
adjust only H+ generated from H2CO3. Furthermore, the kidneys can regulate [HCO3-] in the
body fluids as well. The kidneys compensate for acidosis by secreting excess H + in the urine
while adding new HCO3- to the plasma to expand the HCO3- buffer pool. During alkalosis, the
kidneys conserve H+ by reducing its secretion in the urine. They also eliminate HCO3-, which is in
excess because less HCO3- than usual is tied up buffering H+ when H+ is in short supply.
Secreted H+ that is to be excreted in the urine must be buffered in the tubular fluid to prevent
the H+ concentration gradient from becoming so great that it prevents further H+ secretion.
Normally, H+ is buffered by the urinary phosphate buffer pair, which is abundant in the tubular
fluid because excess dietary phosphate spills into the urine to be excreted from the body. In
acidosis, when all of the phosphate buffer is already used up in buffering the extra secreted H +,
the kidneys secrete NH3 into the tubular fluid to serve as a buffer so that H + secretion can
continue.
•There are four types of acid–base imbalances: respiratory acidosis, respiratory alkalosis,
metabolic acidosis, and metabolic alkalosis. Respiratory acid–base disorders originate with
deviations from normal [CO2], whereas metabolic acid–base imbalances encompass all deviations
in pH other than those caused by abnormal [CO2].