Effect of ph on potassium and proton conductance in renal proximal
tubule.
Gu, Xi, and Henry Sackin.
Dept. of Physiology and Biophysics, Cornell Univ. Medical College,
New York, N.Y. 10021
APStracts 2:0024F, 1995.
The effect of intracellular and extracellular pH on potassium
conductance (GK) was examined in isolated amphibian (Rana Pipiens)
proximal tubule cells under whole-cell voltage clamp conditions.
Internal perfusion of the patch pipette was used to precisely control
intracellular pH. In the region of normal resting potential (-51 +/-
3 mV), raising cell pH from 6.5 to 8.0 did not significantly increase
GK (1.1 +/- 0.3 nS vs. 1.3 +/- 0.3 nS; P > 0.08, n= 8 ). Similar
elevations in external (bath) pH had even less of an effect on GK. In
contrast, when cells were voltage-clamped to 30 mV more negative than
the resting potential, raising internal pH from 6.5 to 8.0 did
increase GK from 1.05 +/- 0.3nS to 1.8 +/- 0.5 nS (P < 0.04; n = 8 ).
These results suggest that modest changes in pH have little effect on
GK, except at large negative potentials. In the process of examining
the pH dependence of GK, a slowly activating, voltage-dependent,
conductance of 7.5 +/- 1nS (n=20; for 20 [mu]m cells) was observed
during cell depolarization. Although the instantaneous I-V relation
of this conductance was linear, its marked voltage dependence
produced an apparent steady state rectification, with Gin = 0.5 +/-
0.2 nS and Gout = 9.0 +/- 1 nS (n=11). Outward current was reversibly
blocked by 3 mM Cu, Cd or Co. In the absence of Na, K, Ca (and only
trace amounts of Cl), rapid changes in bath pH from 6.5 to 8.0
shifted the steady-state reversal potential (Erev) by -37 +/- 4 mV
(n=9) and the instantaneous Erev by -56+/- 4 mV (n=9). These shifts
in Erev were consistent with a hydrogen ion conductance (GH), similar
to what has been reported for snail neuron, neutrophils, alveolar
epithelial cells, and phagocytes. Since the magnitude of this GH
would be insignificant at resting cell pH and membrane potential, its
role in renal proximal tubule under normal conditions is somewhat
obscure. Nonetheless, in pathological situations, GH could function
to prevent acid overload during any process that depolarizes the
cell, such as low temperature or metabolic inhibition.
Received 4 October 1994; accepted in final form 15 February 1995.
APS Manuscript Number F355-4.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 1 March 1995.