Open AccessKATP channels are involved in regulatory volume decrease in rat cardiac myocytes
Author(s) -
Lu Shi,
Meng Xu,
J Liu,
Z Zhang,
Zhijun Bao,
Y Wang,
C Wang,
J Wang
Publication year - 2009
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931594
Subject(s) - glibenclamide , pinacidil , myocyte , chemistry , channel blocker , electrophysiology , potassium channel , atrial myocytes , pharmacology , patch clamp , medicine , biophysics , endocrinology , biology , calcium , diabetes mellitus
Regulatory volume decrease (RVD) is essential for the survival ofanimal cells. The aim of this study was to observe the RVDprocess in rat ventricular myocytes, and to determine if the KATPchannels are involved in the RVD process in these cells. By usingreverse transcriptase polymerase chain reaction and Western blotanalysis, we demonstrated that there are two types of KATPchannels expressed in rat ventricular myocytes: Kir6.1 and Kir6.2.When rat cardiac myocytes were exposed to hypotonic solution,cell volume increased significantly within 15 min and thengradually recovered. This typical RVD process could be inhibitedby a Cl– channel blocker (0.5 mM 9-anthracene-carboxylicacid9-AC), a K+ channel blocker (5.0 mM CsCl) and a KATPchannel blocker glibenclamide (10 µM). Electrophysiologicalresults showed that hypotonic solution activated a whole-cellcurrent, which had similar biophysical characteristics with KATPopener (pinacidil)-induced currents. This current could be blockedby glibenclamide. Our data suggested that the RVD process in ratventricular myocytes is dependent on the activation of K+channels, and that KATP channels are involved in this process.