Journal of Applied Physiology, Vol 51, Issue 6 1630-1634, Copyright © 1981 by American Physiological Society
Myocardial intracellular pH regulation during chloride depletion
N. C. Gonzalez and R. L. Clancy
The possible role of a HCO-3/Cl- transmembrane exchange as a mechanism of
alkalinization in the myocardial cell was studied in isolated rabbit hearts
perfused with Ringer solution. Cl- depletion was produced by replacing Cl-
of the perfusate by SO2(-4) or glucuronate. Intracellular pH (pHi) was
calculated both in Cl--free and Cl--containing hearts from the distribution
of 14C-labeled 5',5'-dimethyloxazolidine-2,4-dione. Acid-base alterations
were produced by changing perfusate HCO-3 concentration and/or CO2 partial
pressure (PCO2). Depletion of Cl- resulted in an increase in pHi for any
given level of extracellular pH. Increasing PCO2 at constant perfusate
HCO-3 resulted in changes in pHi and cell HCO-3 (HCO-3i) that were similar
in both Cl--free and Cl--containing hearts. Increasing perfusate HCO-3 at
constant PCO2 resulted in increases in pHi and HCO-3i in both Cl--free and
Cl--containing preparations. When the increases in HCO-3i secondary to an
increase in extracellular HCO-3 were plotted as a function of the initial
HCO-3i, a significant negative correlation was observed, suggesting that
the elevation of HCO-3i was influenced by the initial HCo-3i and not by the
presence or absence of Cl-. It is concluded that even though HCO-3 may
enter the myocardial cells in exchange for Cl- during Cl-depletion, lack of
Cl- does not alter the ability of the myocardial cell to regulate its pHi.
This argues against a HCO-3/Cl- exchange as a mechanism of regulation of
myocardial pHi.
