AJP - Cell Physiology, Vol 256, Issue 4 C728-C735, Copyright © 1989 by American Physiological Society
Na+-H+ exchange and pH regulation in red blood cells: role of uncatalyzed H2CO3 dehydration
R. Motais, B. Fievet, F. Garcia-Romeu and S. Thomas
Department de Biologie du Commissariat a l'Energie Atomique, Laboratoire Jean Maetz, Villefranche-sur-Mer, France.
Erythrocytes of rainbow trout respond to adrenergic stimulation by
activation of a Na+-H+ exchange. When red blood cells are suspended in
their own plasma and equilibrated with a convenient gas mixture in a
tonometer, the extrusion of H+ induces a fast, very strong acidification of
the blood (by 0.5-0.7 pH units), explained as follows. Excretion of H+ into
a medium containing HCO3- causes the formation of H2CO3. The uncatalyzed
dehydration of H2CO3 is slow so that H+ accumulates above the level that
would prevail at equilibrium, promoting a strong acid disequilibrium pH.
Then the blood pH progressively returns to a value close to its initial
value because of the slow uncatalyzed dehydration of H2CO3 and washout of
the CO2 so produced. The period of acid disequilibrium pH, however, is
lengthened because part of the CO2 generated by the spontaneous dehydration
is not washed out by tonometry but diffuses into the red cells where it is
rapidly converted into HCO3- and H+ by carbonic anhydrase and then excreted
by Na+-H+ and Cl-HCO3- exchangers. This recycling process "refuels" the
ionic reaction, increasing the time needed to reach equilibrium. The anion
exchanger does not sense this strong acid disequilibrium pH, since the
external HCO3- concentration is practically unchanged at that time. During
the extracellular pH (pHe) recovery period, simultaneously extracellular
HCO3- content decreases and intracellular Cl- content increases. Thus
intracellular pH and pHe appear to be uncoupled. This overall
interpretation is confirmed by experiments using carbonic anhydrase and
drugs such as propranolol and amiloride.(ABSTRACT TRUNCATED AT 250 WORDS)
