Relation of membrane potential to basolateral tetraethylammonium transport
in isolated snake proximal renal tubules.
Kim, Yung Kyu, and William H. Dantzler.
Department of Physiology, College of Medicine, University of Arizona,
Tucson, Arizona 85724
APStracts 2:0016R, 1995.
We measured the effects of changes in bath [K+] concentration on
basolateral membrane potential (p.d.) and [3H]tetraethylammonium (TEA)
transport in isolated snake (Thamnophis spp.) proximal renal tubules (25
degrees C; pH 7.4). Increasing bath [K+] from 3 mM to 65 mM decreased p.d.
from -60 mV (inside of cells negative) to -20 mV and 2-min uptake of [3H]TEA
by about 25%, indicating that p.d. influences TEA entry into the cells.
Uptake of [3H]TEA was inhibited similarly at both K+ concentrations by
unlabeled TEA, indicating that uptake is carrier-mediated. Kt (about 18 [mu]M)
for 2-min uptake of [3H]TEA in 3 mM K+ increased significantly in 65 mM
K+, suggesting that the decrease in p.d. or the increase in K+ concentration
alters the affinity of the transporter for TEA. The steady-state cell-to-bath
ratio for [3H]TEA with 3 mM K+ (-60 mV p.d.) was about 16,
significantly above the ratio of 10 predicted for passive distribution at
electrochemical equilibrium. With 65 mM K+ (-20 mV p.d.) this ratio decreased
to about 6, again significantly above the predicted ratio of 2. These data
suggest that the p.d. can account for much, but not all, of the steady-state
uptake of TEA. Efflux of [3H]TEA across the basolateral membrane was
identical with either 3 mM or 65 mM K+ in the bath but was almost completely
inhibited in either case by tetrapentylammonium, a potent inhibitor of TEA
uptake. These data indicate that virtually all TEA transport across the
basolateral membrane is carrier-mediated and that transport out of the cells
is unaffected by p.d.
Received 18 July 1994; accepted in final form 17 January 1995.
APS Manuscript Number R386-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative Comp.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 February 1995.