title: KCNQ channels are involved in the regulatory volume decrease response in primary neonatal rat cardiomyocytes.
abstract: Cardiomyocytes may experience significant cell swelling during ischemia and reperfusion. Such changes in cardiomyocyte volume have been shown to affect the electrical properties of the heart, possibly leading to cardiac arrhythmia. In the present study the regulatory volume decrease (RVD) response of neonatal rat cardiomyocytes was studied in intact single cells attached to coverslips, i.e. with an intact cytoskeleton. The potential contribution of KCNQ (Kv7) channels to the RVD response and the possible involvement of the F-actin cytoskeleton were investigated. The rate of RVD was significantly inhibited in the presence of the KCNQ channel blocker XE-991 (10 and 100 microM). Electrophysiological experiments confirmed the presence of an XE-991 sensitive current and Western blotting analysis revealed that KCNQ1 channel protein was present in the neonatal rat cardiomyocytes. Hypoosmotic cell swelling changes the structure of the F-actin cytoskeleton, leading to a more rounded cell shape, less pronounced F-actin stress fibers and patches of actin. In the presence of cytochalasin D (1 microM), a potent inhibitor of actin polymerization, the RVD response was strongly reduced, confirming a possible role for an intact F-actin cytoskeleton in linking cell swelling to activation of ion transport in neonatal rat cardiomyocytes.
authors: The Danish National Research Foundation Centre for Cardiac Arrhythmia and Department of Biomedical Sciences, The Panum Institute, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark. kirstinec@mfi.ku.dk
authors: Kirstine
authors: K
authors: Calloe
authors: Morten Schak
authors: MS
authors: Nielsen
authors: Morten
authors: M
authors: Grunnet
authors: Nicole
authors: N
authors: Schmitt
authors: Nanna Koschmieder
authors: NK
authors: Jorgensen
mesh_terms: D000199:Actins / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn; D000873:Anthracenes / Q000494:pharmacology; D001145:Arrhythmias, Cardiac / Q000378:metabolism / Q000473:pathology; D002448:Cell Adhesion / Q000187:drug effects; D048429:Cell Size / Q000187:drug effects; D002478:Cells, Cultured; D015638:Cytochalasin D / Q000494:pharmacology; D004553:Electric Conductivity; D017136:Ion Transport / Q000187:drug effects; D051656:KCNQ Potassium Channels / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology; D022502:Stress Fibers / Q000378:metabolism / Q000473:pathology
chemical_list: C112297:10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone; D000199:Actins; D000873:Anthracenes; D051656:KCNQ Potassium Channels; D015638:Cytochalasin D