Electrolyte Balance

IN
THE BODY

Electrolytes include salts, acids, and bases, but the term electrolyte balance usually refers
to the salt balance in the body.
Salts are important in controlling fluid movements and provide minerals essential for
excitability, secretory activity, and membrane permeability.
Although many electrolytes are crucial for cellular activity, here we will specifically
examine the regulation of sodium, potassium, and calcium.
Acids and bases, which are more intimately involved in determining the pH of body fluids,
are considered in the next section.
Salts enter the body in foods and fluids, and small amounts are generated during
metabolic activity.
For example, phosphates are liberated during catabolism of nucleic acids and bone matrix.
Obtaining enough electrolytes is usually not a problem.
Indeed, most of us have a far greater taste than need for salt.
We shake table salt (NaCl) on our food even though natural foods contain ample amounts
and processed foods contain exorbitant quantities.
The taste for very salty foods is learned, but some liking for salt may be innate to ensure
adequate intake of these two vital ions.
Salts are lost from the body in perspiration, feces, and urine.
Even though sweat is normally hypotonic, large amounts of salt can be lost on a hot day
simply because more sweat is produced.
Gastrointestinal disorders can also lead to large salt losses in feces or vomitus.
Thus, the flexibility of renal mechanisms that regulate the electrolyte balance of the blood
is a critical asset.
Some causes and consequences of electrolyte imbalances are summarized in Table 26.1

The Central Role of Sodium in Fluid and
Electrolyte Balance

Sodium holds a central position in fluid and electrolyte balance and overall body homeostasis.
Regulating the balance between sodium input and output is one of the most important renal
functions.
The salts NaHCO
3
and NaCl account for 9095% 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
+
is the single most abundant cation in the
ECF and the only one exerting significant osmotic pressure.
The cellular plasma membrane is relatively impermeable to Na
+
, but some does manage to diffuse in
and must be pumped out against its electrochemical gradient.
These two qualities give sodium the primary role in controlling ECF volume and water distribution in
the body.
It is important to understand that while the sodium content of the body may change, its ECF
concentration normally remains stable because of immediate adjustments in water volume.
Remember, water follows salt.
Furthermore, because all body fluids are in osmotic equilibrium, a change in plasma Na
+
levels affects
not only plasma volume and blood pressure, but also the 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
+
-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 (discussed shortly) are coupled to Na
+
transport.
Regulation of Potassium Balance

Potassium, the chief intracellular cation, is required for normal neuromuscular
functioning as well as for several essential metabolic activities.
Because the relative ICF-ECF potassium concentration directly affects a cells resting
membrane potential, even slight changes in K
+
concentration in the ECF have
profound effects on neurons and muscle fibers that can be extremely dangerous.
K
+
excess in the ECF decreases their membrane potential, causing depolarization,
often followed by reduced excitability.
Too little K
+
in the ECF causes hyperpolarization and nonresponsiveness.
The heart is particularly sensitive to K
+
levels. Both too much and too little K
+

(hyperkalemia and hypokalemia respectively) can disrupt electrical conduction in
the heart, leading to sudden death (Table 26.1).
Potassium is also part of the bodys buffer system, which resists changes in the pH
of body fluids.
Shifts of hydrogen ions (H
+
) into and out of cells induce corresponding shifts of K
+
in
the opposite direction to maintain cation balance.
Thus, ECF potassium levels rise with acidosis, as K
+
leaves and H
+
enters the cells,
and fall with alkalosis, as K
+
moves into the cells and H
+
leaves them to enter the
ECF.
Although these pH-driven shifts do not change the total amount of K
+
in the body,
they can seriously interfere with the activity of excitable cells.

Potassium Regulatory Site: The Cortical
Collecting Duct
Like Na
+
balance, K
+
balance is maintained chiefly by renal mechanisms.
However, there are important differences in the way this balance is achieved.
The amount of Na
+
reabsorbed in the tubules is precisely tailored to need, and Na
+
is never
secreted into the filtrate.
In contrast, the proximal tubules predictably reabsorb about 6080% of the filtered K
+
, and
the thick ascending limb of Henles loop absorbs another 1020% or so, leaving about 10%
to be lost in urine regardless of need.
The responsibility for K
+
balance falls chiefly on the cortical collecting ducts, and is
accomplished mainly by changing the amount of K
+
secreted into the filtrate.
As a rule, K
+
levels in the ECF are sufficiently high that K
+
needs to be excreted, and the
rate at which the principal cells of the cortical collecting ducts secrete K
+
into the filtrate is
accelerated over basal levels.
At times, the amount of K
+
excreted may actually exceed the amount filtered.
When ECF potassium concentrations are abnormally low, K
+
moves from the tissue cells
into the ECF and the renal principal cells conserve K
+
by reducing its secretion and
excretion to a minimum.
Note that these principal cells are the same cells that mediate aldosterone-induced
reabsorption of Na
+
and the ADH-stimulated reabsorption of water.
Additionally, type A intercalated cells, a unique population of collecting duct cells, can
reabsorb some of the K
+
left in the filtrate (in conjunction with active secretion of H
+
), thus
helping to reestablish K
+
(and pH) balance.
However, keep in mind that the main thrust of renal
regulation of K
+
is to excrete it.
Because the kidneys have a limited ability to retain K
+
,
it may be lost in urine even in the face of a deficiency.
Consequently, failure to ingest potassium-rich
substances eventually results in a severe deficiency.
Influence of Plasma Potassium Concentration:
The single most important factor influencing K
+

secretion is the K
+
concentration in blood plasma.
A high-potassium diet increases the K
+
content of the
ECF.
This favors entry of K
+
into the principal cells of the
cortical collecting duct and prompts them to secrete
K
+
into the filtrate so that more of it is excreted.
Conversely, a low-potassium diet or accelerated K
+

loss depresses its secretion (and promotes its limited
reabsorption) by the collecting ducts.

Influence of Aldosterone on Potassium
regulation

The second factor influencing K
+
secretion into the filtrate is
aldosterone.
As it stimulates the principal cells to reabsorb Na
+
, aldosterone
simultaneously enhances K
+
secretion (see Figure 26.8).
Thus, as plasma Na
+
levels rise, K
+
levels fall proportionately.
Adrenal cortical cells are directly sensitive to the K
+
content of the
ECF bathing them.
When it increases even slightly, the adrenal cortex is strongly
stimulated to release aldosterone, which increases K
+
secretion by
the exchange process just described.
Thus, K
+
controls its own concentrations in the ECF via feedback
regulation of aldosterone release.
Aldosterone is also secreted in response to the renin-angiotensin
mechanism previously described.

HOMEOSTATIC IMBALANCE OF
POTASSIUM
In an attempt to reduce NaCl intake, many people
have turned to salt substitutes, which are high in
potassium.
However, heavy consumption of these substitutes is
safe only when aldosterone release in the body is
normal.
In the absence of aldosterone, hyperkalemia is swift
and lethal regardless of K
+
intake (Table 26.1).
Conversely, when a person has an adrenocortical
tumor that pumps out tremendous amounts of
aldosterone, ECF potassium levels fall so low that
neurons all over the body hyperpolarize and paralysis
occurs.