The Kidneys and Regulation of Water and Inorganic Ions
515
SECTION B SUMMARY
Total-Body Balance of Sodium and Water
I. The body gains water via ingestion and internal production,
and it loses water via urine, the gastrointestinal tract, and
evaporation from the skin and respiratory tract (as insensible
loss and sweat).
II. The body gains sodium and chloride by ingestion and loses them
via the skin (in sweat), the gastrointestinal tract, and urine.
III. For both water and sodium, the major homeostatic control
point for maintaining stable balance is renal excretion.
Basic Renal Processes for Sodium and Water
I. Sodium is freely fi lterable at the glomerulus, and its
reabsorption is a primary active process dependent upon Na
+
/
K
+
-ATPase pumps in the basolateral membranes of the tubular
epithelium. Sodium is not secreted.
II. Sodium entry into the cell from the tubular lumen is always
passive. Depending on the tubular segment, it is either
through channels or by cotransport or countertransport with
other substances.
III. Sodium reabsorption creates an osmotic difference across the
tubule, which drives water reabsorption, largely through water
channels (aquaporins).
IV. Water reabsorption is independent of the posterior pituitary
hormone vasopressin until it reaches the collecting duct system,
where vasopressin increases water permeability. A large volume of
dilute urine is produced when plasma vasopressin concentration,
and hence water reabsorption by the collecting ducts, is low.
V. A small volume of concentrated urine is produced by the renal
countercurrent multiplier system when plasma vasopressin
concentration is high.
a. The active transport of sodium chloride by the ascending
loop of Henle causes increased osmolarity of the
Table 14–5
Summary of “Division of Labor” in the Renal Tubules
Tubular Segment
Major Functions
Controlling Factors
Glomerulus/Bowman’s capsule
Forms ultrafi ltrate of plasma
Starling forces (
P
GC
,
P
BS
,
π
GC
)
Proximal tubule
Bulk reabsorption of solutes and water
Secretion of solutes (except potassium)
and organic acids and bases
Active transport of solutes with passive water
reabsorption
Parathyroid hormone inhibits phosphate reabsorption
Loop of Henle
Establishes medullary osmotic gradient
(juxtamedullary nephrons)
Secretion of urea
Descending limb
Bulk reabsorption of water
Passive water reabsorption
Ascending limb
Reabsorption of NaCl
Active transport
Distal tubule and cortical
collecting duct
Fine-tuning of the reabsorption/
secretion of small quantity of solute
remaining
Aldosterone stimulates sodium reabsorption and
potassium excretion
Parathyroid hormone stimulates calcium reabsorption
Cortical and medullary
collecting duct
Fine-tuning of water reabsorption
Reabsorption of urea
Vasopressin increases passive reabsorption of water
Hyperaldosteronism
Hyperaldosteronism
encompasses a variety of chronic diseases
involving an excess of the adrenal hormone aldosterone.
The most common form is
primary aldosteronism,
which
is often due to a noncancerous growth
(
adenoma
)
of the
zona glomerulosa of the adrenal gland. These tumors release
aldosterone in the absence of stimulation by angiotensin II
(they are autonomous). Historically, this was called
Conn’s
syndrome
.
In this condition, plasma aldosterone reaches
very high levels. This stimulates sodium reabsorption and
potassium excretion in the distal portions of the nephron.
ADDITIONAL CLINICAL EXAMPLES
As a result, patients develop hypertension that is diffi cult to
control through standard medications, along with increased
fl uid volume, and low plasma potassium (hypokalemia).
Because of the increased blood pressure and sodium delivery
to the macula densa due to increased fi ltered load of sodium,
renin release is greatly inhibited. Therefore, this is a renin-
independent cause of hypertension and is one of the most
common causes of endocrine hypertension. The usual
treatment of Conn’s syndrome is removal of the adrenal gland
containing the tumor. The remaining adrenal gland then
increases in size in compensation.
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