Cardiac swelling-induced chloride current depolarizes canine atrial
myocytes.
Du, Xiao-Yi, and Steve Sorota.
Department of Pharmacology, Columbia University, 630 West 168th
Street, New York, NY 10032
APStracts 3:0488H, 1996.
The effect of the cardiac swelling-induced chloride current (ICl
-swell) on transmembrane potential was examined. Osmotic swelling
affected resting potassium current through an apparent dilution of
intracellular potassium. Inflating cells by applying positive
pressure to the patch electrode prevented the effect on resting
potassium current. Inflation depolarized dog atrial myocytes when
recording electrodes contained either 17 or 42 mM Cl-. The
depolarization coincided with the activation of ICl-swell and was
antagonized by the chloride channel blocker, niflumic acid.
Substituting extracellular chloride with the more permeant ion, SCN-,
shifted the reversal potential for ICl-swell to more negative values
and antagonized inflation-induced depolarization. The depolarization
was accentuated by replacing extracellular chloride with an less
permeant ion, aspartate. We conclude that activation of ICl-swell in
atrial cells causes significant depolarization of the resting
membrane. The outward rectification of ICl-swell and the high cell
membrane resistance during the action potential plateau suggest that
ICl-swell will also have significant effects on atrial action
potential configuration.
Received 16 May 1996; accepted in final form 7 November 1996.
APS Manuscript Number H447-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996