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Dogs with compensated biventricular hypertrophy due to chronic atrioventricular block (cAVB), are more susceptible to develop drug-induced Torsade-de-Pointes arrhythmias and sudden cardiac death. It has been suggested that the increased Na +  influx in hypertrophied cAVB ventricular myocytes contribute to these lethal arrhythmias. The increased Na +  influx was not mediated by Na +  channels, in fact the Na +  current proved reduced in cAVB myocytes. Here we tested the hypothesis that increased activity of the Na + /H +  exchanger type 1 (NHE-1), commonly observed in hypertrophic hearts, causes the elevated Na +  influx. Cardiac acid-base transport was studied with a pH-sensitive fluorescent dye in ventricular myocytes isolated from control and hypertrophied cAVB hearts; the H +  equivalent flux through NHE-1, Na + -HCO −  3  cotransport (NBC), Cl − /OH −  exchange (CHE), and Cl − /HCO −  3  exchange (AE) were determined and normalized per liter cell water and corrected for surface-to-volume ratio. In cAVB, sarcolemmal NHE-1 flux was increased by 65 ± 6.3% in the pH  i   interval 6.3–7.2 and NBC, AE, and CHE fluxes remained unchanged. Accordingly, at steady-state intracellular pH the total sarcolemmal Na +  influx by NHE-1 + NBC increased from 8.5 ± 1.5 amol/μm 2 /min in normal myocytes to 15 ± 2.4 amol/μm 2 /min in hypertrophied cAVB myocytes. We conclude that compensated cardiac hypertrophy in cAVB dogs is accompanied with an increased sarcolemmal NHE-1 activity. This in conjunction with unchanged activity of the other acid-base transporters will raise the intracellular Na +  in hypertrophied cAVB myocytes.

Increased sarcolemmal Na+/H+ exchange activity in hypertrophied myocytes from dogs with chronic atrioventricular block