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E-4031 enhanced Ca2+ transient and ventricular myocytes contraction via reverse mode Na+/Ca2+ exchange in normal and
Xiang-Li Cui1, Lu-Ying Zhao, Bo-Wei Wu
1Department of Physiology, Shanxi Medical University, Taiyuan 030001, China. xianglic@sohu.com
Aim:
To study the effects of N-[4-[[1-[2-(6-methyl-2-pyridinyl)ethyl]-4-piperidinyl]carbonyl]phenyl]methanesulfonamide dihydrochloride dihydrate (E-4031), a specific Ik blocker, on Ca2+ transient and cell contraction of normal and hypertrophied rat ventricular myocytes.
Methods:
Electrically triggered Ca2+ transient and cell shortening were measured simultaneously using the Ion Imaging System with charge coupled digital (CCD) camera.
Results:
E-4031 (10 micromol/L) increased Ca2+ transient and cell shortening from (210+/-49) and (3.0+/-0.8) micron to (245+/-47) and (3.6+/-1.0) micron, respectively (P<0.05) in normal cardiomyocytes and from (196+/-54) and (3.0+/-1.3) micron to (240+/-49) and (3.6+/-1.3) micron respectively (P<0.05) in hypertrophied cardiomyocytes, while did not change calcium sensitivity in both groups. KB-R7943 completely blocked the activating effects induced by E-4031 in both of normal and hypertrophied cardiomyocytes. Nicardipine did not block the increasing effects of E-4031.
Conclusion:
E-4031 increased Ca2+ transient and cell contraction via stimulating reverse mode of Na+/Ca2+ exchange while without influencing calcium sensitivity. These effects were more notable in hypertrophied cardiomyocytes than in normal myocytes.