Water, Electrolytes, and Acid-Base Balance
F IG U R E 39-1
Proportional distribution of solids and water in a healthy adult.
2. Active reabsorption (principally in the proximal
tubule) of solutes from the glomerular filtrate; and
3. Active excretion of substances such as hydrogen ions
into the tubular lumen, usually in the distal portion of
the tubule (Figure 39-3).
100-120 mL/min; about 150 L of fluid passes through
the renal tubules each day. Since the average daily urine
volume is 1
-1.5 L, 99% of the glomerular filtrate is reab-
sorbed. Approximately 80% of the water is reabsorbed in
the proximal tubule, a consequence of active absorption
of solutes. Reabsorption in the rest of the tubule varies ac-
cording to the individual’s water balance, in contrast to the
o b lig a to r y
reabsorption that occurs in the proximal tubule.
The facultative absorption of water depends on the es-
tablishment in the loop of Henle of an osmotic gradient
Phosphate and sulfate
C a T
F IG U R E 3 9 -2
Composition of body fluids.
by the secretion of Na+ from the ascending loop and their
uptake by the descending loop. As a result, the proximal
end of the loop is hyperosmotic
( 1 2 0 0
mosm/kg) and the
distal end hypoosmotic with respect to blood. The col-
lecting ducts run through the hyperosmotic region. In the
absence of antidiuretic hormone (ADH; see Chapter 31),
the cells of the ducts are relatively impermeable to water.
They become permeable to water in the presence of ADH,
however, and the urine becomes hyperosmotic with respect
39.2 Homeostatic Controls
The composition and volume of extracellular fluid are
regulated by complex hormonal and nervous mechanisms
that interact to control its osmolality, volume, and pH.
The osmolality of extracellular fluid is due mainly to
Na+ and accompanying anions. It is kept within nar-
row limits (285-295 mosm/kg) by regulation of water
intake (via a thirst center) and water excretion by the
kidney through the action of ADH. The volume is kept
relatively constant, provided the individual’s weight re-
mains constant to within ±1 kg. Volume receptors sense
the effective circulating blood volume, which when de-
creased, stimulates the renin-angiotensin-aldosterone sys-
tem and results in retention of Na+ (Chapter 32). The
increased Na+ level leads to a rise in osmolality and se-
cretion of ADH, with a resultant increase in water re-
tention. Antagonistic systems exist that result in an in-
creased Na+ excretion.
Atrial natriuretic peptide
also called atrial natriuetic factor or hormone, is released
by the cardiocytes of the cardiac atria in response to me-
chanical stretch caused by the plasma volume expansion.
ANF induces diuresis and natriuresis. These effects re-
sult from renal hemodynamic changes associated with in-
creases in GFR and inhibition of Na+ reabsorption from
inner medullary collecting ducts. ANP is a 28-amino-acid
peptide and has a single disulfide linkage (Figure 39-4).
The precursor and the storage form of ANP in cardiocytes
is a 126-amino-acid polypeptide. Some of the stimuli other
than the blood volume which function as secretogosues of
ANP include high blood pressure, elevated serum osmo-
lality, increased heart rate, and elevated levels of plasma
catecholamines. Activation of the ANP gene in cardio-
cytes by glucocorticoids leads to increased synthesis of
ANP. ANP also regulates Na+ and water homeostasis by
different mechanisms that include inhibition of steps in
the renin-angiotensin-aldosterone pathway and inhibition
of ADH secretion from posterior pituitary cells.
The mechanism of action of ANP on target cells in-
volves the formation of cGMP via the activation of plasma