The Kidneys and Regulation of Water and Inorganic Ions
503
gland and known as
vasopressin,
or
antidiuretic hormone,
(ADH).
Vasopressin stimulates the insertion into the luminal
membrane of a particular group of aquaporin water channels
made by the collecting duct cells. Thus, in the presence of a
high plasma concentration of vasopressin, the water permea-
bility of the collecting ducts increases dramatically. Therefore,
water reabsorption is maximal, and the fi nal urine volume is
small—less than 1 percent of the fi ltered water.
Without vasopressin, the water permeability of the col-
lecting ducts is extremely low, and very little water is reab-
sorbed from these sites. Therefore, a large volume of water
remains behind in the tubule to be excreted in the urine. This
increased urine excretion resulting from low vasopressin is
termed
water diuresis.
Diuresis
simply means a large urine
fl ow from any cause. In a subsequent section, we will describe
the control of vasopressin secretion.
The disease
diabetes insipidus,
which is distinct from the
other kind of diabetes (diabetes mellitus, or “sugar diabetes”),
illustrates what happens when the vasopressin system malfunc-
tions. Diabetes insipidus is caused by the failure of the posterior
pituitary to release vasopressin
(
central diabetes insipidus
),
or
the inability of the kidney to respond to vasopressin
(
nephro-
genic diabetes insipidus
).
Regardless of the type of diabetes
insipidus, the permeability to water of the collecting ducts is
low even if the patient is dehydrated. A constant water diuresis
is present that can be as much as 25 L/day.
Note that in water diuresis, there is an increased urine
fl ow, but not an increased solute excretion. In all other cases
of diuresis, termed
osmotic diuresis,
the increased urine
fl ow is the result of a primary increase in solute excretion. For
example, failure of normal sodium reabsorption causes both
increased sodium excretion and increased water excretion,
because, as we have seen, water reabsorption is dependent
on solute reabsorption. Another example of osmotic diuresis
occurs in people with uncontrolled
diabetes
mellitus:
In this
case, the glucose that escapes reabsorption because of the
huge fi ltered load retains water in the lumen, causing it to be
excreted along with the glucose.
To summarize, any loss of solute in the urine must be
accompanied by water loss (osmotic diuresis), but the reverse
is not true. That is, water diuresis is not necessarily accompa-
nied by equivalent solute loss.
Urine Concentration: The Countercurrent
Multiplier System
Before reading this section you should review, by looking
up in the glossary, several terms presented in Chapter 4—
hypoosmotic, isoosmotic,
and
hyperosmotic.
In the section just concluded, we described how the kid-
neys produce a small volume of urine when the plasma con-
centration of vasopressin is high. Under these conditions, the
urine is concentrated (hyperosmotic) relative to plasma. This
section describes the mechanisms by which this hyperosmo-
larity is achieved.
The ability of the kidneys to produce hyperosmotic urine
is a major determinant of the ability to survive with limited
water intake. The human kidney can produce a maximal uri-
nary concentration of 1400 mOsmol/L, almost fi ve times the
osmolarity of plasma, which is typically in the range of 285 to
300 mOsmol/L (rounded off to 300 mOsmol/L for conve-
nience). The typical daily excretion of urea, sulfate, phosphate,
other waste products, and ions amounts to approximately 600
mOsmol. Therefore, the minimal volume of urine water in
which this mass of solute can be dissolved equals
600 mOsmol/day
= 0.444 L/day
1400 mOsmol/L
This volume of urine is known as the
obligatory water loss.
The loss of this minimal volume of urine contributes to dehy-
dration when water intake is zero.
Urinary concentration takes place as tubular fl uid fl ows
through the
medullary
collecting ducts. The interstitial fl
uid
surrounding these ducts is very hyperosmotic. In the presence
of vasopressin, water diffuses out of the ducts into the inter-
stitial fl uid of the medulla and then enters the blood vessels of
the medulla to be carried away.
The key question is: how does the medullary interstitial
fl uid become hyperosmotic? The answer involves several inter-
related factors: 1. The countercurrent anatomy of the loop of
Henle of juxtamedullary nephrons; 2. Reabsorption of NaCl in
the ascending limbs of those loops of Henle; 3. Impermeability
of those ascending limbs to water; 4. Trapping of urea in the
medulla; and 5. Hairpin loops of vasa recta to minimize wash-
out of the hyperosmotic medulla. Recall that Henle’s loop
forms a hairpin-like loop between the proximal tubule and the
distal convoluted tubule (see Figure 14–2). The fl
uid entering
the loop from the proximal tubule fl ows down the descending
limb, turns the corner, and then fl ows up the ascending limb.
The opposing fl ows in the two limbs is termed a countercur-
rent fl ow, and the entire loop functions as a
countercurrent
multiplier system
to create a hyperosmotic medullary inter-
stitial fl
uid.
Because the proximal tubule always reabsorbs sodium and
water in the same proportions, the fl uid entering the descend-
ing limb of the loop from the proximal tubule has the same
osmolarity as plasma—300 mOsmol/L. For the moment, let’s
skip the descending limb because the events in it can only be
understood in the context of what the
ascending
limb is doing.
Along the entire length of the ascending limb, sodium and
chloride are reabsorbed from the lumen into the medullary
interstitial fl
uid (
Figure 14–16a
). In the upper (thick) portion
of the ascending limb, this reabsorption is achieved by trans-
porters that actively cotransport sodium and chloride. Such
transporters are not present in the lower (thin) portion of the
ascending limb, so the reabsorption there is a passive process.
For simplicity in the explanation of the countercurrent mul-
tiplier, we shall treat the entire ascending limb as a homoge-
neous structure that actively reabsorbs sodium and chloride.
Very importantly,
the ascending limb is relatively imper-
meable to water,
so that little water follows the salt. The net
result is that the interstitial fl uid of the medulla becomes
hyperosmotic compared to the fl uid in the ascending limb
because solute is reabsorbed without water.
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