Cardiac swelling-induced chloride current depolarizes canine atrial myocytes

• Published in: The American journal of physiology Vol. 272; no. 4 Pt 2; p. H1904
• Main Authors: Du, X Y, Sorota, S
• Format: Journal Article
• Language: English
• Published: United States 01.04.1997
• Subjects: Action Potentials; Animals; Barium - pharmacology; Cells, Cultured; Chloride Channels - drug effects; Chloride Channels - physiology; Chlorides - pharmacology; Dogs; Electric Conductivity; Heart - physiology; Heart Atria; Heart Ventricles; Hypotonic Solutions; Membrane Potentials - drug effects; Niflumic Acid - pharmacology; Osmolar Concentration; Patch-Clamp Techniques; Thiocyanates - pharmacology
• ISSN: 0002-9513
• DOI: 10.1152/ajpheart.1997.272.4.h1904

The effect of the cardiac swelling-induced chloride current (I(Cl,swell)) on the transmembrane potential was examined. Osmotic swelling affected the resting potassium current through an apparent dilution of intracellular potassium. Inflating cells by applying positive pressure to the patch electrode prevented the effect on the resting potassium current. Inflation depolarized dog atrial myocytes when the recording electrodes contained either 17 or 42 mM Cl-. The depolarization coincided with activation of I(Cl,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 I(Cl,swell) to more negative values and antagonized inflation-induced depolarization. The depolarization was accentuated by replacing extracellular chloride with a less permeant ion, aspartate. We conclude that activation of I(Cl,swell) in atrial cells causes significant depolarization of the resting membrane. The outward rectification of I(Cl,swell) and the high cell membrane resistance during the action potential plateau suggest that I(Cl,swell) will also have significant effects on atrial action potential configuration.