Protein kinase C enhances the swelling-induced chloride current in human atrial myocytes.
10.1007/s11596-016-1596-5
- Author:
Ye-Tao LI
1
;
Xin-Ling DU
2
Author Information
1. Department of Cardiovascular Surgery, Guizhou Provincial People's Hospital, Guiyang, 550002, China.
2. Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. 46176992@qq.com.
- Publication Type:Journal Article
- Keywords:
atrial myocyte/human;
protein kinase C;
swelling-activated chloride current;
whole-cell patch-clamp technique
- MeSH:
Anthracenes;
pharmacology;
Chloride Channels;
metabolism;
Chlorides;
agonists;
antagonists & inhibitors;
metabolism;
Culture Media;
metabolism;
pharmacology;
Dose-Response Relationship, Drug;
Evoked Potentials;
drug effects;
physiology;
Heart Atria;
cytology;
drug effects;
metabolism;
Humans;
Hypotonic Solutions;
metabolism;
pharmacology;
Indoles;
pharmacology;
Ion Transport;
drug effects;
Maleimides;
pharmacology;
Myocytes, Cardiac;
cytology;
drug effects;
metabolism;
Patch-Clamp Techniques;
Phorbol 12,13-Dibutyrate;
pharmacology;
Primary Cell Culture;
Protein Kinase C;
metabolism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2016;36(3):383-388
- CountryChina
- Language:English
-
Abstract:
Swelling-activated chloride currents (ICl.swell) are thought to play a role in several physiologic and pathophysiologic processes and thus represent a target for therapeutic approaches. However, the mechanism of ICl.swell regulation remains unclear. In this study, we used the whole-cell patch-clamp technique to examine the role of protein kinase C (PKC) in the regulation of ICl.swell in human atrial myocytes. Atrial myocytes were isolated from the right atrial appendages of patients undergoing coronary artery bypass and enzymatically dissociated. ICl.swell was evoked in hypotonic solution and recorded using the whole-cell patch-clamp technique. The PKC agonist phorbol dibutyrate (PDBu) enhanced ICl.swell in a concentration-dependent manner, which was reversed in isotonic solution and by a chloride current inhibitor, 9-anthracenecarboxylicacid. Furthermore, the PKC inhibitor bis-indolylmaleimide attenuated the effect and 4α-PDBu, an inactive PDBu analog, had no effect on ICl.swell. These results, obtained using the whole-cell patch-clamp technique, demonstrate the ability of PKC to activate ICl,swell in human atrial myocytes. This observation was consistent with a previous study using a single-channel patch-clamp technique, but differed from some findings in other species.
