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An increased TREK-1-like potassium current in ventricular myocytes during rat cardiac hypertrophy.

Authors: Wang, W  Zhang, M  Li, P  Yuan, H  Feng, N  Peng, Y  Wang, L  Wang, X 
Citation: Wang W, etal., J Cardiovasc Pharmacol. 2013 Apr;61(4):302-10. doi: 10.1097/FJC.0b013e318280c5a9.
Pubmed: (View Article at PubMed) PMID:23232841
DOI: Full-text: DOI:10.1097/FJC.0b013e318280c5a9

To elucidate the expression and identify the functional changes of 2 pore domain potassium channel TREK-1 during cardiac hypertrophy in rats, left ventricular hypertrophy was induced by subcutaneous injection with isoproterenol. Western blot was used to detect the expression of TREK-1 channel protein, and inside-out and whole-cell recordings were used to record TREK-1 currents. The results showed that TREK-1 protein expression in endocardium was slightly higher than that in epicardium in control left ventricles. However, it was obviously upregulated by 89.8% during hypertrophy, 2.3-fold higher than in epicardium. Mechanical stretch, intracellular acidification, and arachidonic acid could activate a TREK-1-like current in cardiomyocytes. The slope conductances of cardiac TREK-1 and CHO/TREK-1 channels were 123 +/- 7 and 113 +/- 17 pS, respectively. The TREK-1 inhibitor L-3-n-butylphthalide (10 muM) reduced the currents in CHO/TREK-1 cells, normal cardiomyocytes, and hypertrophic cardiomyocytes by 48.5%, 54.3%, and 55.5%, respectively. The percentage of L-3-n-butylphthalide-inhibited outward whole-cell current in hypertrophic cardiomyocytes (23.7%) was larger than that in normal cardiomyocytes (14.2%). The percentage of chloroform-activated outward whole-cell current in hypertrophic cardiomyocytes (58.3%) was also larger than normal control (40.2%). Our results demonstrated that in hypertrophic rats, TREK-1 protein expression in endocardium was specifically increased and the ratio of TREK-1 channel current in cardiac outward currents was also enhanced. TREK-1 might balance potassium ion flow during hypertrophy and might be a potential drug target for heart protection.


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CRRD Object Information
CRRD ID: 9831114
Created: 2015-02-25
Species: All species
Last Modified: 2015-02-25
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.