The Kidneys and Regulation of Water and Inorganic Ions
and muscle. Recall from Chapter 6 that the resting membrane
potentials of these tissues are directly related to the rela-
tive intracellular and extracellular potassium concentrations.
Consequently, either increases
or decreases
in extracellular potassium concentration can
cause abnormal rhythms of the heart
abnormalities of skeletal muscle contraction.
A healthy person remains in potassium balance in the
steady state by daily excreting an amount of potassium in the
urine equal to the amount ingested minus the amounts elimi-
nated in feces and sweat. Like sodium, potassium losses via
sweat and the gastrointestinal tract are normally quite small,
although vomiting or diarrhea can cause large quantities to be
lost. The control of urinary potassium excretion is the major
mechanism regulating body potassium.
Renal Regulation of Potassium
Potassium is freely fi lterable in the renal corpuscle. Normally,
the tubules reabsorb most of this fi ltered potassium so that very
little of the fi ltered potassium appears in the urine. However,
the cortical collecting ducts can secrete potassium, and changes
in potassium excretion are due mainly to changes in potassium
secretion by this tubular segment (
Figure 14–28
During potassium depletion, when the homeostatic
response is to minimize potassium loss, there is no potas-
sium secretion by the cortical collecting ducts. Only the small
amount of fi ltered potassium that escapes tubular reabsorp-
tion is excreted. With normal fl
uctuations in potassium intake,
a variable amount of potassium is added to the small amount
fi ltered and not reabsorbed. This maintains total-body potas-
sium balance.
Figure 14–14b illustrates the mechanism of potassium
secretion by the cortical collecting ducts. In this tubular seg-
ment, the K
pumped into the cell across the basolateral mem-
brane by Na
-ATPases diffuses into the tubular lumen
through K
channels in the luminal membrane. Thus, the
secretion of potassium by the cortical collecting duct is
associated with the reabsorption of sodium by this tubular
segment. Potassium secretion does not occur in other sodium-
reabsorbing tubular segments because there are few potas-
sium channels in the luminal membranes of their cells.
Rather, in these segments, the potassium pumped into the
cell by Na
-ATPase simply diffuses back across the baso-
lateral membrane through potassium channels located there
(see Figure 14–14a).
What factors infl uence potassium secretion by the cortical
collecting ducts to achieve homeostasis of bodily potassium?
The single most important factor is as follows: When a high-
potassium diet is ingested (
Figure 14–29
), plasma potassium
concentration increases, though very slightly, and this drives
enhanced basolateral uptake via the Na
-ATPase pumps.
Thus, there is an enhanced potassium secretion. Conversely,
a low-potassium diet or a negative potassium balance, such
as results from diarrhea, lowers basolateral potassium uptake.
This reduces potassium secretion and excretion, thereby help-
ing to reestablish potassium balance.
A second important factor linking potassium secretion
to potassium balance is the hormone aldosterone (see Figure
14–29). Besides stimulating tubular sodium reabsorption
by the cortical collecting ducts, aldosterone simultane-
ously enhances tubular potassium secretion by this tubular
The homeostatic mechanism by which an excess or defi cit
of potassium controls aldosterone production (see Figure 14–29)
is different from the mechanism described earlier involving
the renin-angiotensin system. The aldosterone-secreting cells
of the adrenal cortex are sensitive to the potassium concen-
tration of the extracellular fl uid. Thus, an increased intake of
Dry mouth,
Metering of water
intake by GI tract
Figure 14–27
Inputs controlling thirst. The osmoreceptor input is the single most
important stimulus under most physiological conditions. Psychological
factors and conditioned responses are not shown. The question mark (?)
indicates that evidence for the effects of angiotensin II on thirst comes
primarily from experimental animals.
Proximal tubule
and loop of Henle
collecting duct
in urine
Figure 14–28
Simplifi ed model of the basic renal processing of
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