|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS
1Laboratory of Physiology, Hasselt University, Diepenbeek, Belgium; 2Laboratory of Physiology, K. U. Leuven Campus Gasthuisberg O & N, Leuven, Belgium; 3Laboratory of Biophysics, International Centre of Biodynamics, Bucharest, Romania; 4Department of Health and Environmental Physics, Horia Hulubei National Institute for Physics and Nuclear Engineering, Bucharest, Romania
Submitted 12 June 2005 ; accepted in final form 9 August 2005
In this study, we have investigated the dependence of Na+ transport regulation on membrane cholesterol content in A6 renal epithelia. We continuously monitored short-circuit current (Isc), transepithelial conductance (GT), and transepithelial capacitance (CT) to evaluate the effects of cholesterol extraction from the apical and basolateral membranes in steady-state conditions and during activation with hyposmotic shock, oxytocin, and adenosine. Cholesterol extraction was achieved by perfusing the epithelia with methyl-
-cyclodextrin (m
CD) for 1 h. In steady-state conditions, apical membrane cholesterol extraction did not significantly affect the electrophysiological parameters; in contrast, marked reductions were observed during basolateral m
CD treatment. However, apical m
CD application hampered the responses of Isc and GT to hypotonicity, oxytocin, and adenosine. Analysis of the blocker-induced fluctuation in Isc demonstrated that apical m
CD treatment decreased the epithelial Na+ channel (ENaC) open probability (Po) in the steady state as well as after activation of Na+ transport by adenosine, whereas the density of conducting channels was not significantly changed as confirmed by CT measurements. Na+ transport activation by hypotonicity was abolished during basolateral m
CD treatment as a result of reduced Na+/K+ pump activity. On the basis of the findings in this study, we conclude that basolateral membrane cholesterol extraction reduces Na+/K+ pump activity, whereas the reduced cholesterol content of the apical membranes affects the activation of Na+ transport by reducing ENaC Po.
epithelial Na+ channel; Na+-K+-ATPase activity; short-circuit current; methyl-
-cyclodextrin; channel open probability
This article has been cited by other articles:
![]() |
W. G. Hill, M. B. Butterworth, H. Wang, R. S. Edinger, J. Lebowitz, K. W. Peters, R. A. Frizzell, and J. P. Johnson The Epithelial Sodium Channel (ENaC) Traffics to Apical Membrane in Lipid Rafts in Mouse Cortical Collecting Duct Cells J. Biol. Chem., December 28, 2007; 282(52): 37402 - 37411. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Starke-Peterkovic, N. Turner, M. F. Vitha, M. P. Waller, D. E. Hibbs, and R. J. Clarke Cholesterol Effect on the Dipole Potential of Lipid Membranes Biophys. J., June 1, 2006; 90(11): 4060 - 4070. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |