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Proximal Convoluted Tubule
The Na-K-ATPase on the basolateral membrane of the PCT cells moves sodium
out of the cells creating a lowered intracellular sodium concentration.
This provides an impetus for the sodium in the PCT lumen to move into the
cells via a sodium-proton antiporter. In exchange, protons are sent
into the lumen where they combine with bicarbonate ions to form carbonic
acid.
DCT
In the DCT, a luminal carbonic acid anhydrase converts the carbonic acid
into H2O and CO2 which can enter DCT cells.
Here they are back-converted by a second carbonic anhydrase. Protons
are actively secreted in the DCT by a sodium-independent electrogenic ATPase,
while the bicarbonate is recovered. The protons are buffered in the
urine by "titratable" acids, primarily inorganic phosphate, with some contribution
from others such as urate and creatinine.
CT
The kidney can control pH to some extent by regulation of titratable acid.
In states of acidosis, more phosphate is secreted to help buffer the load
(leading to hypophosphatemia) while alkalosis promotes phosphate reabsorbtion.
Ammonia production can augment proton excretion on an as-needed basis.
Glutamine is converted in collecting tubute (CT) cells into ammonium and
bicarbonate. The ammonium is exchanged with sodium in the lumen,
and the ammonium remains charge-trapped in the lumen. The bicarbonate
from the breakdown of glutamine is reabsorbed. Any ammonium
that is not excreted is reabsorbed into circulation, and this is problematic
because it is toxic. In the liver ammonium can be detoxified by conversion
to urea, a process which consumes bicarbonate. Both hypercalcemia
and hyperkalemia inhibit renal ammonium excretion. |
