CONSEQUENCES OF CO2 ACIDOSIS FOR TRANSMEMBRANE NA+ TRANSPORT AND MEMBRANE CURRENT IN RABBIT CARDIAC PURKINJE-FIBERS

1. The influence of sarcolemmal Na(+)‐H+ exchange on intracellular Na+ activity (aiNa), intracellular pH (pHi) and membrane holding current (Ih) was investigated in rabbit cardiac Purkinje fibres. pHi and aiNa were measured with liquid sensor ion‐selective microelectrodes. A two‐microelectrode voltage clamp was used while recording pHi or aiNa.pHi was varied by alternating a nominally CO2‐free HEPES buffer and a CO2‐HCO3‐buffer. 2. The intrinsic buffer capacity was calculated from the decrease in pHi after addition of CO2. The most accurate estimate was obtained when transmembrane pHi regulation was blocked and equalled 18.4 +/‐ 1.0 mequiv H+/pH unit (mean +/‐ S.E.M.). 3. aiNa started to rise when pHi fell below 7.0. A hyperpolarization paralleled the increase in aiNa. The magnitude of the rise in aiNa and the hyperpolarization were steeply dependent on pHi. 4. Inhibition of the Na(+)‐K+ pump by K(+)‐free superfusion increased aiNa. The rate of rise in aiNa was highly dependent on pHi. The rates of rise in 5% (pHi = 7.00 +/‐ 0.03), 7% (pHi = 6.89 +/‐ 0.04) and 15% CO2 (pHi = 6.74 +/‐ 0.02) at constant external pH (pHo) relative to the rate in HEPES solution (pHi = 7.24 +/‐ 0.02) were: 1.5 +/‐ 0.2, 2.4 +/‐ 0.1 and 3.1 +/‐ 0.2. The acid‐induced rise in aiNa was abolished by 2 mM‐amiloride. 5. Extracellular acidosis slowed down the recovery of pHi and depressed the rate of rise in aiNa upon intracellular acidification. When both pHi and pHo were decreased to 6.7 the acid‐dependent rate increase fell to about 10% of the value found at pHo 7.4. 6. The tetrodotoxin (TTX)‐sensitive Na+ current was not influenced by the change in pHi in the range 6.7‐7.2. 7. Intracellular acidosis was associated with an early aiNa‐independent depolarization and an inward shift in Ih. Current‐voltage plots revealed that the initial inward current shift reversed at ‐81.5 mV on average, showed inward rectification and was largely depressed in the presence of 1 mM‐Ba2+. These observations indicate a decrease in K+ conductance when pHi falls. 8. The increase in aiNa elicited a Na(+)‐K+ pump‐dependent outward current which could override the initial aiNa‐independent current shift. At a pHo of 6.7 the initial fall in Ih remained, while the secondary outward current was largely depressed. 9. The rate of active Na+ extrusion and Na(+)‐K+ pump current were suppressed by about 30% at pHi 6.7 compared to pHi 7.2.(ABSTRACT TRUNCATED AT 400 WORDS) © 1990 The Physiological Society