Hypertonicity Decreases Basolateral K+ and Cl− Conductances in Rabbit Proximal Convoluted Tubule

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 (V BL) 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, V BL further depolarizes to reach a steady depolarization of 19.5 ± 1.5 mV (n= 15) with respect to control. In the post-control period, V BL returns to −55.8 ± 1.5 mV. The basolateral partial conductance to K+ (t K ) 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− (t Cl), 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 (t NaHCO3), 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 (G Na-HCO3) does not vary appreciably. Concomitant with cell shrinkage, intracellular pH (pH i ) 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 pH i 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Hypertonicity Decreases Basolateral K+ and Cl− Conductances in Rabbit Proximal Convoluted Tubule

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Publisher
Springer-Verlag
Copyright
Copyright © Inc. by 1997 Springer-Verlag New York
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s002329900175
Publisher site
See Article on Publisher Site

Abstract

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 (V BL) 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, V BL further depolarizes to reach a steady depolarization of 19.5 ± 1.5 mV (n= 15) with respect to control. In the post-control period, V BL returns to −55.8 ± 1.5 mV. The basolateral partial conductance to K+ (t K ) 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− (t Cl), 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 (t NaHCO3), 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 (G Na-HCO3) does not vary appreciably. Concomitant with cell shrinkage, intracellular pH (pH i ) 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 pH i 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.

Journal

The Journal of Membrane BiologySpringer Journals

Published: Feb 1, 1997

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