AJP - Cell Physiology, Vol 258, Issue 6 C1117-C1126, Copyright © 1990 by American Physiological Society
Role of Na(+)-H+ and Cl(-)-HCO3- antiports in the regulation of cytosolic pH near neutrality
T. I. Tonnessen, K. Sandvig and S. Olsnes
Institute for Cancer Research, Norwegian Radium Hospital, Oslo.
In Vero cells, Na(+)-H+ antiport as well as Na(+)-coupled and
Na(+)-independent Cl(-)-HCO3- antiport are involved in regulation of
cytosolic pH (pHi) after large (unphysiological) deviations from
neutrality. In this paper we have studied to which extent each of the three
antiports is involved in regulation of pHi after small deviations from
neutrality expected to occur under physiological conditions. At
physiological extracellular pH (pHo), inhibition of Na(+)-H+ exchange by
amiloride did not alter pHi. At neutral and alkaline pHo, pHi was found to
be lower in the presence of HCO3- than in its absence, whereas at acidic
pHo, pHi was higher in the presence of HCO3- than in its nominal absence.
Above pHi 6.5, the activity of the Na(+)-coupled Cl(-)-HCO3- antiport was
higher than the Na(+)-H+ antiport. After a small reduction of pHi, the
recovery of steady-state pHi was entirely dependent on Na(+)-coupled
Cl(-)-HCO3- antiport, whereas after more pronounced acidification, also
Na(+)-H+ exchange contributed to the acid extrusion. The Na(+)-independent
Cl(-)-HCO3- antiport, which acts as an acidifying mechanism, was strongly
activated at pHi greater than 7.1. The results indicate that at
physiological pHo the steady-state pHi is largely determined by the
activity of the two Cl(-)-HCO3- antiports, and they suggest that Na(+)-H+
exchange does not influence the resting pHi under these conditions.
