Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Cell Physiol 266: C42-C51, 1994;
0363-6143/94 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fermini, B.
Right arrow Articles by Nattel, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fermini, B.
Right arrow Articles by Nattel, S.

AJP - Cell Physiology, Vol 266, Issue 1 C42-C51, Copyright © 1994 by American Physiological Society


ARTICLES

Choline chloride activates time-dependent and time-independent K+ currents in dog atrial myocytes

B. Fermini and S. Nattel
Montreal Heart Institute, Department of Medicine, University of Montreal, Quebec, Canada.

Using the whole cell configuration of the patch-clamp technique, we studied the effect of isotonic replacement of bath sodium chloride (NaCl) by choline chloride (ChCl) in dog atrial myocytes. Our results show that ChCl triggered 1) activation of a time-independent background current, characterized by a shift of the holding current in the outward direction at potentials positive to the K+ equilibrium potential (EK), and 2) activation of a time- and voltage-dependent outward current, following depolarizing voltage steps positive to EK. Because the choline-induced current obtained by depolarizing steps exhibited properties similar to the delayed rectifier K+ current (IK), we named it IKCh. The amplitude of IKCh was determined by extracellular ChCl concentration, and this current was generally undetectable in the absence of ChCl. IKCh was not activated by acetylcholine (0.001-1.0 mM) or carbachol (10 microM) and could not be recorded in the absence of ChCl or when external NaCl was replaced by sucrose or tetramethylammonium chloride. IKCh was inhibited by atropine (0.01-1.0 microM) but not by the M1 antagonist pirenzepine (up to 10 microM). This current was carried mainly by K+ and was inhibited by CsCl (120 mM, in the pipette) or barium (1 mM, in the bath). We conclude that in dog atrial myocytes, ChCl activates a background conductance comparable to ACh-dependent K+ current, together with a time-dependent K+ current showing properties similar to IK.


This article has been cited by other articles:


Home page
Mol. Pharmacol.Home page
H. Shi, H. Wang, and Z. Wang
Identification and Characterization of Multiple Subtypes of Muscarinic Acetylcholine Receptors and Their Physiological Functions in Canine Hearts
Mol. Pharmacol., March 1, 1999; 55(3): 497 - 507.
[Abstract] [Full Text]


Home page
J. Pharmacol. Exp. Ther.Home page
J. Feng, Z. Wang, G.-R. Li, and S. Nattel
Effects of Class III Antiarrhythmic Drugs on Transient Outward and Ultra-rapid Delayed Rectifier Currents in Human Atrial Myocytes
J. Pharmacol. Exp. Ther., April 1, 1997; 281(1): 384 - 392.
[Abstract] [Full Text]


Home page
Circ. Res.Home page
D. Qin, Z.-H. Zhang, E. B. Caref, M. Boutjdir, P. Jain, and N. El-Sherif
Cellular and Ionic Basis of Arrhythmias in Postinfarction Remodeled Ventricular Myocardium
Circ. Res., September 1, 1996; 79(3): 461 - 473.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online