AJP - Renal Physiology, Vol 259, Issue 2 348-F356, Copyright © 1990 by American Physiological Society
Hypotonic shock activates a maxi K+ channel in primary cultured proximal tubule cells
L. Dube, L. Parent and R. Sauve
Departement de Physiologie, Universite de Montreal, Quebec, Canada.
The nature and function of the ionic channels at the apical membrane of
primary cultured proximal tubule cells (PT) was investigated by use of the
extracellular patch-clamp method. Several types of ionic channels were
observed, including a calcium-dependent K+ channel of 206 pS in symmetrical
162 mM KCl activated at depolarizing potentials [maxi K+(Ca2+)]. Whole cell
experiments were also carried out that clearly indicated that the PT cells
respond to a hypotonic shock by activating electroconductive pathways. This
response consisted of an initial hyperpolarization (from -47 to -58 mV, SD
= 3, n = 4), followed by a strong depolarization (to -23 mV, SD = 4, n =
4). Furthermore, it was found in cell-attached experiments that the maxi
K+(Ca2+) channel becomes activated during the hypotonic challenge. The
activation process required external Ca2+, although some residual
single-channel activity was measured in the absence of extracellular
calcium (n = 3). On the basis of these results, it is concluded that the
volume regulation process in PT cells in response to a hypotonic shock
involves an influx of calcium from the external medium, which in turn
triggers the opening of apical maxi K+(Ca2+) channels.
