NA-INDEPENDENT CL--HCO3- EXCHANGE MEDIATES RECOVERY OF PH(I) FROM ALKALOSIS IN GUINEA-PIG VENTRICULAR MYOCYTES

The pH-sensitive fluorescent indicator, carboxy-seminaphthorhodafluor 1 (SNARF 1) was used to assess the contribution of forward Na-independ ent Cl--HCO3- exchange (1 external Cl- exchanged for 1 internal HCO3-) to intracellular pH (pH(i)) recovery from alkalosis in adult ventricu lar myocytes (guinea pig). Intracellular alkalosis was elicited by ext ernal application of the weak base, trimethylamine. In the absence of CO2-HCO3- (N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffere d solution) the initial rate of pH(i) recovery from alkalosis (pH(i) a pproximate to 7.25-7.75) was slow and independent of pH(i), yielding a n apparent net HCO3- efflux of 0.36 +/- 0.11 mM/min. In CO2-HCO3--buff ered solution, the initial rate of pH(i) recovery and net HCO3- efflux were much faster and markedly increased by raising pH(i). At pH(i) ap proximate to 7.25, net HCO3- efflux was similar to 2 mM/min and rose t o 9 mM/min at pH(i) approximate to 7.6. 4,4'-Diisothiocyanostilbene-2, 2'-disulfonic acid (0.4 mM) decreased net HCO3- efflux by 78.1 +/- 8.9 % in CO2-HCO3--buffered solution. Reduction in extracellular Cl- conce ntration from 135 to 20 mM markedly slowed the rate of pH(i) recovery from alkalosis and reduced net HCO3- efflux. pH(i) recovery from alkal osis was unaffected by removal of external sodium or exposure to 1 mM amiloride. These results indicate that forward Na-independent Cl--HCO3 - exchange mediates pH(i) recovery from alkalosis in guinea pig ventri cular myocytes.