On the nature of delayed repolarization during sustained sodium coupled transport in frog proximal tubules

In proximal tubules of the frog kidney, stimulation of coupled transport of sodium with phenylalanine leads to depolarization of the cell membrane, followed by repolarization within a few minutes. The repolarization is due to a delayed increase of potassium conductance at the peritubular cell membrane. The present study was designed to test for the role of depolarization, of calmodulin and of arachidonic acid metabolites for the delayed increase of potassium conductance. To this end, the potential difference across the peritubular cell membrane of proximal convoluted tubules (PD_pt) has been recorded continuously during exposure of the lumen to phenylalanine or during galvanic current injection into a neighbouring cell. During control conditions, PD_pt averages –68.6±1.0 mV (n=45). Phenylalanine leads to a depolarization of the peritubular cell membrane by +31.5±1.3 mV (n=20), followed by a repolarization by –12.9±1.1 mV (n=20) within 3 min. Injection of currents from 10 to 80 nAmps leads to a depolarization by + 0.83±0.01 mV/nAmps which is again followed by repolarization. A linear correlation is observed between the magnitude of depolarization (dep) and repolarization (rep)within 3 min: rep (mV)= –(0.24±0.01) dep (mV) + (2.45±0.12) mV (r=0.09). Thus, depolarization is capable to trigger delayed repolarization. The extent of repolarization is a function of the magnitude of depolarization. The possible involvement of calmodulin or arachidonic acid metabolites has been tested for by inducing sodium coupled transport in the presence of 100 mol/l mepacrine, 10 mol/l indomethacin or 10 mol/l trifluoperazine. As a result, indomethacin and trifluoperazine do not significantly interfere with either depolarization or repolarization of the cell membrane during stimulation of sodium coupled transport while mepacrine significantly reduces repolarization.