Regulation of Proximal Renal Tubular K+ Conductance by Intracellular pH

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Abstract
Conventional electrophysiology and 2’, 7’-bis-(2-carboxyethyl)-5-(and 6)-carboxyfluorescein fluorescence have been applied to elucidate the effects of metabolic acidosis on straight proximal tubules of the mouse kidney. Reduction of extracellular bicarbonate concentration from 20 to 10 mmol/l leads to a decline of intracellular pH from 7.00+0.06 to 6.85 ± 0.05, a depolarization of the cell membrane (PDb1) from –72 ± 1 to -59 ± 2 mV, a decrease of the basolateral transference number for potassium (tK) from 0.80 ± 0.01 to 0.54 ± 0.03, an increase of the basolateral transference number for bicarbonate (tb) from 0.16 ± 0.02 to 0.42 ± 0.03 and an increase of the fractional resistance of the basolateral over the luminal cell membrane (Rb/Ra) by 64 ± 8%. Upon return to 20 mmol/l bicarbonate after a 5-min exposure to 10 mmol/l bicarbonate, the intracellular pH approached a more alkaline value (7.28 ± 0.08) than before exposure to acidosis. Despite the intracellular alkalosis, PDb1 (-67 ± 1 mV) and tK (0.73 ± 0.02) remained significantly below, and tb (0.26 ± 0.02) and Rb/Ra (32 ± 8%) significantly above the respective values before induction of acidosis. Even transient exposure of the tubules to 40 mmol/l extracellular bicarbonate did not restore the original electrophysiological properties of the tubule cells. It is concluded that both a rapidly reversible and a long-lasting decrease of proximal tubular K+ conductance follows cellular acidosis.

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