Page 255 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

246 ACID-BASE DISORDERS

WHOLE-BODY REGULATION of a luminal Na -H antiporter (NHE3) and approxi-
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OF ACID-BASE BALANCE mately one third by a luminal vacuolar or V-type H -
33
adenosinetriphosphatase (H -ATPase). The H ,K -
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Acid-base balance requires the cooperation of three major ATPase found in the luminal membranes of the type A
organs: liver, kidneys, and lungs. By the process of alveo- intercalated cells of the collecting ducts is quantitatively
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lar ventilation, the lungs remove the tremendous amount less important for H secretion but mediates K reab-
of volatile acid (10,000 to 15,000 mmol CO 2 ) produced sorption. These transport mechanisms depend on the
each day by metabolic processes. The liver metabolizes presence of carbonic anhydrase in tubular cells. Carbonic
amino acids derived from protein catabolism to glucose anhydrase II is found in the cytoplasm, where it catalyzes
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or triglyceride and releases NH 4 in the process. When the recombination of CO 2 and H 2 O into H 2 CO 3 , and
þ carbonic anhydrase IV is tethered to the luminal mem-
urea is synthesized in the liver from NH 4 and CO 2 ,
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H is produced and HCO 3 is titrated. Consequently, brane where it facilitates conversion of H 2 CO 3 to CO 2

the liver produces much of the fixed or nonvolatile acid and H 2 O in tubular fluid (Fig. 9-6). Of the filtered

that must be excreted each day. The kidneys excrete HCO 3 , 80% is reabsorbed in the proximal tubule, 10%
þ in the thick ascending limb of Henle’s loop. 6% in the dis-
NH 4 in the urine, thus diverting it from ureagenesis

and producing a net gain of HCO 3 and net loss of H . tal convoluted tubule, and 4% in the collecting duct
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(Fig. 9-7).
RENAL REGULATION OF IfsecretedH titratesfilteredHCO 3 ,HCO 3 iseffec-

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ACID-BASE BALANCE tively reabsorbed because one HCO 3 is added to ECF

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for each filtered HCO 3 titrated by a secreted H (see
The kidneys maintain normal ECF HCO 3 concentra- Fig. 9-6). This process occurs primarily in the proximal

tion by reabsorbing virtually all filtered HCO 3 and by tubules. Net acid excretion and generation of “new”

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regenerating HCO 3 that has been titrated during the HCO 3 occur whenever secreted H titrates phosphate
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daily endogenous production of fixed, or nonvolatile, in tubular fluid or whenever NH 4 is excreted in the urine
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acid. The latter process is accomplished by excretion of with Cl or in exchange for Na (Figs. 9-8 and 9-9). These
titratable acidity (primarily phosphate salts) and ammo- processes occur primarily in the distal nephron.
nium salts. The term net acid excretion is defined as the
FACTORS AFFECTING RENAL
sum of titratable acidity and ammonium minus HCO 3 BICARBONATE REABSORPTION
in the urine. Normally, there is a negligible amount of

HCO 3 in urine. If the glomerular filtration rate (GFR) and ECF volume

All three of the functions described above are accom- (ECFV) are constant, the amount of HCO 3 reabsorbed
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plished by renal tubular secretion of H . Approximately by the kidneys is equal to the filtered load. Under these

two thirds of hydrogen ion secretion occurs by means conditions, HCO 3 appears to have a tubular maximum
Tubular fluid Proximal tubule cell Interstitial fluid
Interstitial
Tubular fluid Collecting duct cell fluid
Na + Na + Na +
Filtered H + H + HCO 3 – 3HCO – Reclaimed
HCO – 3 HCO 3 – Cl –
3 ATP
Filtered H + H + HCO 3 –
HCO – Reclaimed
H CO H CO 3
2 3 2 3 –
HCO 3
H CO H CO
2 3 2 3
CA CA 3Na +
ATP CA 3Na +
H O CO CO + H O 2K + ATP
2
2
2
2
H O CO CO + H O 2K +
2 2 2 2
A B
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Figure 9-6 A and B, Reabsorption of filtered HCO3 by H ion secretion in the proximal tubule. CA,
Carbonic anhydrase. (Drawing by Tim Vojt.)