Effect of temperature on peritubular cell membrane potential and potassium conductance in isolated perfused proximal tubules of the mouse

Abstract

In order to test for the effect of temperature on the electrical properties of renal tubule cells, electrophysiological measurements were made in segments of proximal straight tubules of the mouse, which were dissected free and perfused in vitro. The transepithelial potential difference was −1.6±0.1 mV ( n = 29). The potential difference across the peritubular cell membrane ( U m,bl ) recorded with microelectrodes, amounts to −62 ± 1 mV ( n = 118). Rapid increases of peritubular potassium concentration from 5 to 20 mmol/dm 3 lead to a depolarization of the basolateral cell membrane (Δ U m,bl by +24 ± 1 mV ( n = 103) which is indicative for a high relative potassium conductance of the basolateral cell membrane. Rapid cooling leads to an initial hyperpolarization from −61 ± 1 mV to −65 ± 1 mV ( n = 33) followed by a gradual decline of U m,bl . A parallel decline of Δ U m,bl indicates that the depolarization is at least partially due to decreasing peritubular potassium conductance. Rewarming causes a transient depolarization from −61±1 to −34±2 mV ( n = 20) followed by a complete repolarization within 1 minutes. Phlorizin hyperpolarizes U m,bl from −59±2 to −66±1 mV ( n = 13) and blunts the hyperpolarizing effect of hypothermia and the depolarizing effect of rewarming. Ouabain, like hypothermia, leads to a parallel decline of U m,bl and Δ U m,bl . In conclusion, inhibition of the sodium/potassium-ATPase by hypothermia or ouabain leads to a significant reduction of the peritubular potassium conductance which leads to the depolarization of U m,bl In addition, hypothermia inhibits the sodium-coupled glucose transport across the luminal cell membrane, an effect which tends to hyperpolarize the cell membrane.