Regulation of intracellular pH in smooth muscle cells of the guinea‐pig femoral artery.

1. Intracellular pH (pHi) of smooth muscle cells in isolated strips of guinea‐pig femoral artery was measured using double‐barrelled pH‐sensitive microelectrodes. 2. In modified Krebs solution equilibrated with 5% CO2, pHi was 7.26 +/‐ 0.14 (n = 36; mean +/‐ S.D. of an observation) and the membrane potential (Em) was ‐60.5 +/‐ 5.5 mV. Removal of CO2 from the superfusing solution caused an immediate transient alkalosis before pHi stabilized at much the same value (7.28 +/‐ 0.14; n = 16) as in the presence of CO2. 3. The rate of recovery of pHi from experimentally induced acidosis was not measurably affected by the presence or nominal absence of CO2‐HCO3‐. 4. Application of amiloride (100 microM) blocked recovery from acidosis in the nominal absence of CO2‐HCO3‐ and caused a progressive fall in pHi. In the presence of CO2‐HCO3‐, application of amiloride allowed a slow recovery to pHi 6.7‐7.0, but completely prevented full recovery to the normal pHi. 5. Removal of extracellular Na+ (Na+o) caused a dramatic, progressive fall in pHi in both the presence and nominal absence of CO2‐HCO3‐. 6. The amiloride‐insensitive extrusion of acid equivalents observed in the presence of CO2‐HCO3‐ to pHi 6.7‐7.0 was inhibited by removal of Na+o but was not affected by preequilibration with DIDS (see Methods). 7. It is concluded that Na(+)‐H+ exchange is largely responsible for the effective extrusion of acid equivalents in these arterial cells, at least from relatively small perturbations. A DIDS‐insensitive, Na(+)‐ and HCO3(‐)‐dependent mechanism provides some recovery from acidosis to a relatively low pHi. 8. Comparison with data obtained in exactly the same manner in smooth muscle cells of the guinea‐pig ureter indicates that there are significant differences in the regulation of pHi in different smooth muscles.