The Kidneys and Regulation of Water and Inorganic Ions
519
tion eliminates or replenishes hydrogen ions was stated earlier.
That is, the excretion of a bicarbonate in the urine increases
the plasma hydrogen ion concentration just as if a hydrogen
ion had been added to the plasma. Similarly, the addition of
a bicarbonate to the plasma lowers the plasma hydrogen ion
concentration just as if a hydrogen ion had been removed from
the plasma.
Thus, when the plasma hydrogen ion concentration
decreases (alkalosis) for whatever reason, the kidneys’ homeo-
static response is to excrete large quantities of bicarbonate. This
increases plasma hydrogen ion concentration toward nor-
mal. In contrast, when plasma hydrogen ion concentration
increases (acidosis), the kidneys do not excrete bicarbonate in
the urine. Rather, kidney tubular cells produce
new
bicarbon-
ate and add it to the plasma. This lowers the plasma hydrogen
ion concentration toward normal.
Bicarbonate Handling
Bicarbonate is completely fi lterable at the renal corpuscles
and undergoes signifi cant tubular reabsorption in the proxi-
mal tubule, ascending loop of Henle, and cortical collecting
ducts. Bicarbonate can also be secreted in the collecting ducts.
Therefore:
HCO
3
excretion =
HCO
3
fi ltered + HCO
3
secreted – HCO
3
reabsorbed
For simplicity, we will ignore the secretion of bicarbonate
because it is always much less than tubular reabsorption, and
we will treat bicarbonate excretion as the difference between
ltration and reabsorption.
Bicarbonate reabsorption is an active process, but it is not
accomplished in the conventional manner of simply having an
active pump for bicarbonate ions at the luminal or basolateral
membrane of the tubular cells. Instead, bicarbonate reabsorp-
tion depends on the tubular secretion of hydrogen ions, which
combine in the lumen with fi ltered bicarbonates.
Figure 14–31
illustrates the sequence of events. Begin
this fi
gure inside the cell with the combination of CO
2
and
H
2
O to form H
2
CO
3
, a reaction catalyzed by the enzyme car-
bonic anhydrase. The H
2
CO
3
immediately dissociates to yield
H
+
and bicarbonate (HCO
3
). The HCO
3
diffuses down its
concentration gradient across the basolateral membrane into
interstitial fl uid and then into the blood. Simultaneously, the
H
+
is secreted into the lumen. Depending on the tubular seg-
ment, this secretion is achieved by some combination of pri-
mary H
+
-ATPase pumps, primary H
+
/K
+
-ATPase pumps, and
Na
+
/H
+
countertransporters.
The secreted H
+
, however, is not excreted. Instead, it
combines in the lumen with a fi ltered HCO
3
and generates
CO
2
and H
2
O, both of which can diffuse into the cell and
be available for another cycle of hydrogen ion generation. The
overall result is that the bicarbonate fi ltered from the plasma at
the renal corpuscle has disappeared, but its place in the plasma
has been taken by the bicarbonate that was produced inside
the cell. In this manner, no net change in plasma bicarbonate
concentration has occurred. It may seem inaccurate to refer to
this process as bicarbonate “reabsorption” because the bicar-
bonate that appears in the peritubular plasma is not the same
bicarbonate ion that was fi ltered. Yet, the overall result is the
same as if the fi ltered bicarbonate had been reabsorbed in the
conventional manner like a sodium or potassium ion.
Except in response to alkalosis, discussed in the next
section, the kidneys normally reabsorb all fi ltered bicarbonate,
thereby preventing the loss of bicarbonate in the urine.
Addition of New Bicarbonate to the Plasma
An essential concept shown in Figure 14–31 is that as long as
there are still signifi cant amounts of fi ltered bicarbonate ions in
the lumen, almost all secreted hydrogen ions will combine with
them. But what happens to any secreted hydrogen ions once
almost all the bicarbonate has been reabsorbed and is no longer
available in the lumen to combine with the hydrogen ions?
The answer, illustrated in
Figure 14–32
, is that the
extra secreted hydrogen ions combine in the lumen with a fi l-
tered nonbicarbonate buffer, usually HPO
4
2–
. (Other fi ltered
buffers can also participate, but HPO
4
2–
is the most impor-
tant.) The hydrogen ion is then excreted in the urine as part
of an H
2
PO
4
ion. Now for the critical point: note in Figure
14–32 that, under these conditions, the bicarbonate generated
within the tubular cell by the carbonic anhydrase reaction and
entering the plasma constitutes a
net gain
of bicarbonate by
the plasma, not merely a replacement for a fi ltered bicarbonate.
Thus, when a secreted hydrogen ion combines in the lumen
Tubular
lumen
Tubular epithelial
cells
Interstitial fluid
HCO
3
(filtered)
HCO
3
+ H
+
HCO
3
HCO
3
H
2
CO
3
H
2
O + CO
2
H
2
O + CO
2
H
2
CO
3
H
+
Carbonic
anhydrase
Begin
Figure 14–31
Reabsorption of bicarbonate. Begin looking at this fi
gure inside
the cell, with the combination of CO
2
and H
2
O to form H
2
CO
3
.
As shown in the fi
gure, active H
+
-ATPase pumps are involved in
the movement of H
+
out of the cell across the luminal membrane;
in several tubular segments, this transport step is also mediated by
Na
+
/H
+
countertransporters and/or H
+
/K
+
-ATPase pumps.
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