Chapter 26
Fluid, Electrolyte, and Acid-Base Balance
999
26
in these two variables trigger a variety of neural and hormonal
controls that regulate total body Na
1
content.
Influence of Aldosterone and Angiotensin II
Te hormone
aldosterone
“has the most to say” about renal
regulation of sodium ions. But whether aldosterone is present
or not, some 65% of the Na
1
in the renal filtrate is reabsorbed
in the proximal tubules of the kidneys and another 25% is re-
claimed in the nephron loops (see Chapter 25).
When aldosterone concentrations are high, essentially
all
the remaining filtered Na
1
is actively reabsorbed in the distal
convoluted tubules and collecting ducts. Consistent with aldo-
sterone’s central role in maintaining blood volume and blood
pressure, water always follows Na
1
. Tis water comes from ei-
ther the intracellular fluid or, if ADH is present, from the fil-
trate in the collecting ducts. One way or another, aldosterone
increases ECF volume.
When aldosterone release is inhibited, virtually no Na
1
re-
absorption occurs beyond the distal convoluted tubule. Urinary
excretion of large amounts of Na
1
always
results in the excre-
tion of large amounts of water as well, but the reverse is
not
true. Substantial amounts of nearly sodium-free urine can be
eliminated as needed to achieve water balance.
Te most important trigger for aldosterone release from the
adrenal cortex is the renin-angiotensin-aldosterone mechanism
mediated by the juxtaglomerular complex (JGC) of the renal
tubules. In addition, elevated K
1
concentration in the ECF can
directly stimulate adrenal cortical cells to release aldosterone
(Figure 26.8)
Te result of aldosterone release is increased reabsorption of
Na
1
and increased secretion of K
1
. Aldosterone brings about its
effects slowly, over a period of hours to days. Te principal ef-
fects of aldosterone are to decrease urinary output and increase
blood volume.
Low blood volume and blood pressure (reflecting decreased
body Na
1
content) trigger renin release from the granular cells
of the JGC in three ways shown in Figure 26.10: (1) sympathetic
stimulation, (2) decreased filtrate NaCl concentration, or (3) de-
creased stretch of the granular cells. Renin catalyzes the initial
step in the reactions that produce angiotensin II. Angiotensin II
renal functions. Te salts NaHCO
3
and NaCl account for 90–
95% of all solutes in the ECF, and they contribute about 280
mOsm of the total ECF solute concentration (300 mOsm).
At its normal plasma concentration of about 142 mEq/L,
Na
1
is the single most abundant cation in the ECF and the only
one exerting
significant
osmotic pressure. Additionally, cellular
plasma membranes are relatively impermeable to Na
1
(some
does manage to diffuse in and must be pumped out against its
electrochemical gradient). Tese two qualities give sodium the
primary role in controlling ECF volume and water distribution
in the body.
Remember:
Water follows salt
. Because all body fluids are
in osmotic equilibrium, a change in plasma Na
1
levels affects
not only plasma volume and blood pressure, but also ICF and
IF volumes. In addition, sodium ions continuously move back
and forth between the ECF and body secretions. For example,
about 8 L of Na
1
-containing secretions (gastric, intestinal, and
pancreatic juice, saliva, bile) are spewed into the digestive tract
daily, only to be almost completely reabsorbed. Finally, renal
acid-base control mechanisms (which we will discuss shortly)
are coupled to Na
1
transport.
Sodium Concentration Versus Sodium Content
For ions other than Na
1
, their concentration in body fluids is
the only important variable. For Na
1
, however, both the con-
centration and the total body content are important.
Concentration of Na
1
.
Te concentration of Na
1
in the ECF
largely determines the osmolality of ECF fluids and influ-
ences electrical excitability of neurons and muscles. Te con-
centration of Na
1
normally remains relatively stable because
water immediately moves by osmosis into or out of the ICF,
counteracting the change in Na
1
concentration. In the long
term, the ADH and thirst mechanisms control the ECF Na
1
concentration by controlling water loss or gain.
Content of Na
1
.
Te total body content of Na
1
determines
the ECF volume and therefore blood pressure. Na
1
content
is regulated by the renin-angiotensin-aldosterone and atrial
natriuretic peptide (ANP) hormone mechanisms that con-
trol Na
1
reabsorption and excretion (Na
1
balance). We will
review these mechanisms in the next section.
It helps to think about these aspects of Na
1
balance as sepa-
rate and distinct because they have different roles in homeosta-
sis
(Table 26.2)
. Nevertheless, there is some overlap between
them and their mechanisms are intertwined. For example, as
ECF Na
1
content increases, ECF osmolality rises as well, which
triggers the ADH and thirst mechanisms. Tis increases water
retention and intake, simultaneously reducing the Na
1
concen-
tration and increasing the ECF volume.
Regulation of Sodium Balance
Despite the crucial importance of sodium, receptors that specif-
ically monitor the concentration or content of Na
1
in body flu-
ids have yet to be found. Because regulation of the Na
1
balance
is inseparably linked to blood volume and pressure, changes
Table 26.2
Sodium Concentration
and Sodium Content
 
ECF Na
1
CONCENTRATION
BODY Na
1
CONTENT
Homeostatic
Importance
ECF osmolality
Blood volume and
blood pressure
Sensors
Osmoreceptors
Baroreceptors
Regulation
ADH and thirst
mechanisms
Renin-angiotensin-
aldosterone and
ANP hormone
mechanisms*
*ADH and thirst are also required to maintain blood volume and for long-
term control of blood pressure.
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