AJP - Cell Physiology, Vol 256, Issue 4 C764-C771, Copyright © 1989 by American Physiological Society
Evidence for apical sodium channels in frog lung epithelial cells
H. Fischer, W. Van Driessche and W. Clauss
Institut fur Veterinarphysiologie, Freie Universitat Berlin, Federal Republic of Germany.
To reveal the mechanism of Na+ transport across Xenopus lung epithelium, we
recorded short-circuit current (Isc), transepithelial resistance (Rt), and
current noise spectra while the isolated lung tissues were mounted in an
Ussing-type chamber. Mean values of Isc and Rt obtained while the tissue
was bilaterally incubated with NaCl-Ringer solution were Isc = 11.57 +/-
1.19 microA.cm-2 and Rt = 0.82 +/- 0.07 k omega.cm2. Amiloride added to the
mucosal (apical) side depressed Isc by 61 to 99%. Ouabain abolished Isc
totally when added to the basolateral compartment. Adenosine 3',5'-cyclic
monophosphate (cAMP), epinephrine, and a variety of other compounds did not
alter Isc significantly. Transepithelial depolarization with serosal KCl
solution reduced Isc to 6.22 +/- 1.37 microA.cm-2. Amiloride-sensitive
current and the kinetics of amiloride interaction were not significantly
affected by depolarization. Fluctuation analysis of Isc in the presence of
amiloride revealed a Lorentzian component in the power density spectrum
indicating apical Na+ channels. Assuming pseudo-first order kinetics, we
calculated single channel currents (iNa) and channel density (M): iNa =
0.29 +/- 0.04 pA and M = 0.24 +/- 0.04 micron 2. Our results show that the
route for Na+ transport through lung epithelial cells follows the classical
Koefoed-Johnson-Ussing model for tight epithelia.
