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Cardiovascular Research 2001 51(1):59-70; doi:10.1016/S0008-6363(01)00279-6
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Ionic basis for membrane potential changes induced by hypoosmotic stress in guinea-pig ventricular myocytes

Ivan Kocic, Yuji Hirano and Masayasu Hiraoka*

Department of Cardiovascular Diseases and Etiology and Pathogenesis Research Unit, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan

* Corresponding author. Tel.: +81-3-5803-5829; fax: +81-3-5684-6295 hiraoka.card{at}mri.tmd.ac.jp

Objective: Causal relation between changes in action potentials and activation of several ionic currents during hypoosmotic challenge was investigated. Methods: We recorded changes in membrane potentials and currents during hypotonic stress in guinea-pig ventricular myocytes using whole-cell patch-clamp technique. Results: Exposure of ventricular myocytes to hypotonic solution (0.6 T) caused initial prolongation (~107% of control) of action potential duration at 90% repolarization (APD90) in 65% of examined myocytes. Later shortening (~75% of control) of APD90 and depolarization of resting potential (RP) (~ 4 mV) developed in all cells. Initial prolongation of APD90 in hypotonic solution was mainly caused by transient activation of Gd3+-sensitive non-selective cation (NSC) current. Late changes after ~180 s in hypotonic solution were sustained increase in slow component of delayed rectifier K+ current (IKs) in all cells, and activation of IClswell in 40% of cells. Prevention of APD90 shortening by chromanol, a selective blocker of IKs, was seen in about 40% of myocytes due to short APD in our experimental conditions. Application of 1 mM anthracene-9-carboxylic acid (9-AC) partially inhibited APD shortening in three of seven cells. Depolarization of RP was unaffected by the above-mentioned drugs, but was dependent on [K+]o. Conclusions: Initial prolongation followed by later shortening of APD in hypotonic solution are mostly caused by different sequences of NSC, IKs and IClswell currents activation. Depolarization of RP in hypotonic solution is probably due to dilution of subsarcolemmal K+ concentration and/or change in permeability ratio for Na+ and K+.

KEYWORDS Cl-channel; Ion channels; K-channel; Arrythmia (mechanisms); Membrane potential; Repolarization; Stretch/m–e coupling


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