Hypertonicity decreases basolateral K+ and Cl- conductances in rabbit proximal convoluted tubule.

Collapsed proximal convoluted tubules (PCT) shrink to reach a volume 20% lower than control and do not exhibit regulatory volume increase when submitted to abrupt 150 mOsm/kg hypertonic shock. The shrinking is accompanied by a rapid depolarization of the basolateral membrane potential (VBL) of 8.4 +/- 0.5 mV, with respect to a control value of -54.5 +/- 1.9 mV (n = 15). After a small and transient hyperpolarization, VBL further depolarizes to reach a steady depolarization of 19.5 +/- 1.5 mV (n = 15) with respect to control. In the post-control period, VBL returns to -55.8 +/- 1.5 mV. The basolateral partial conductance to K+ (tK) which is 0.17 +/- 0.01 (n = 5) in control condition, decreases rapidly to nonmeasurable values during the hypertonic shock and returns to 0.23 +/- 0.03 in the post-control period. The basolateral partial conductance to Cl- (tCl), which is 0.05 +/- 0.02 (n = 5) in control, also decreases in hypertonicity to a nonmeasurable value and returns to 0.03 +/- 0.01 in post control. The partial conductance mediated by the Na-HCO3 cotransporter (tNaHCO3), which is 0.48 +/- 0.06 (n = 5) in control condition, remains the same at 0.44 +/- 0.05 (n = 5) during the hypertonic period. Similarly, the membrane absolute conductance mediated by the Na-HCO3 cotransporter (GNa-HCO3) does not vary appreciably. Concomitant with cell shrinkage, intracellular pH (pHi) decreases from a control value of 7.26 +/- 0.01 to 7.13 +/- 0.02 (n = 12) and then remains constant. Return to control solution brings back pHi to 7.28 +/- 0.03. From these results, we conclude that in collapsed PCT, a sustained decrease in cellular volume leads to cell acidification and to inhibition of K+ and Cl- conductances.