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Osmosensitive properties of rapid and slow delayed rectifier K + currents in guinea‐pig heart cells
Author(s) -
Ogura Toshitsugu,
Matsuda Hiroyuki,
Shibamoto Toshishige,
Imanishi Sunao
Publication year - 2003
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2003.03869.x
Subject(s) - osmotic concentration , myocyte , biophysics , intracellular , chemistry , hyperpolarization (physics) , medicine , stimulation , endocrinology , osmotic shock , biology , biochemistry , organic chemistry , nuclear magnetic resonance spectroscopy , gene
Summary 1. Changes in cell volume affect a variety of sarcolemmal transport processes in the heart. To study whether osmotically induced cell volume shrinkage has functional consequences for K + channel activity, guinea‐pig cardiac preparations were superfused with hyperosmotic Tyrode's solution (1.2–2‐fold normal osmolality). Membrane currents and cell surface dimensions were measured from whole‐cell patch‐clamped ventricular myocytes and membrane potentials were recorded from isolated ventricular muscles and non‐patched myocytes. 2. Hyperosmotic treatment of myocytes quickly (< 3 min to steady state) shrank cell volume (approximately 20% reduction in 1.5‐fold hyperosmotic solution) and depressed the delayed rectifier K + current ( I K ). Analysis using different activation protocols and a selective inhibitor (5 µmol/L E4031) indicated that the I K inhibition was due to osmolality and cell volume‐dependent changes in the two subtypes of the classical cardiac I K (rapidly activating I Kr and slowly activating I Ks ); 1.5‐fold hyperosmotic treatment depressed the amplitudes of I Kr and I Ks by approximately 30 and 50%, respectively. 3. Superfusion of muscles and myocytes with 1.5‐fold hyperosmotic solution lengthened the action potentials by 14–17%. Hyperosmotic treatment also caused 6–7 mV hyperpolarization that is most likely due to a concentrating of intracellular K + . 4. The inhibition of I K helps explain the lengthening of action potentials observed in osmotically stressed heart cells. These results, together with the reported I K stimulation by hyposmotic cell swelling, provide further support for cell volume‐sensitive properties of cardiac electrical activity.