Expressions of L-type calcium channel and potassium channel Kv4.3 in rapid paced primary cultured atrial myocytes.
- Author:
Wei CHENG
1
;
Ying-bin XIAO
;
Xue-feng WANG
;
Lin CHEN
;
Qian-jin ZHONG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Atrial Fibrillation; metabolism; physiopathology; Calcium Channels, L-Type; metabolism; Cardiac Pacing, Artificial; Cells, Cultured; Myocytes, Cardiac; metabolism; RNA, Messenger; metabolism; Rats; Rats, Wistar; Shal Potassium Channels; metabolism
- From: Chinese Journal of Cardiology 2006;34(4):312-315
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the expressions of L-type calcium channel alpha1c and potassium channel Kv4.3 at early stages of atrial fibrillation in a rapid paced primary cultured atrial myocyte model.
METHODSPrimary rat atrial myocytes were cultured and a rapid paced cell model was established. The atrial cells were divided into five groups with pacing durations within 0 and 24 h. Reverse transcription-polymerase chain reaction and Western blot were applied to detect the messenger ribonucleic acid (mRNA) and proteins of L-type calcium channel alpha1c and potassium channel Kv4.3, respectively.
RESULTSmRNA expression of L-type calcium channel alpha1c reduced after 6 h of rapid pacing and continued to decline as the pacing process. The decrease of L-type calcium channel alpha1c protein was paralleled with mRNA expression and reached the lowest levels at 24 h. Similarly, changes of potassium channel Kv4.3 protein and mRNA were paralleled. Kv4.3 mRNA was not altered within the first 6 h. It was reduced after 12 h. However, longer pacing periods did not further decrease mRNA and protein expression levels of potassium channel Kv4.3.
CONCLUSIONSExpressions of L-type calcium channel alpha1c and potassium channel Kv4.3 were both reduced at different levels in early phase of rapid pacing atrial myocytes. It implicates the occurrence of ion channel remodeling of atrial myocytes, which may serve as molecular mechanism of electrical remodeling in the development of atrial fibrillation.