Research

Mechano-Electro-Transduction

The heart is an electro-mechanical pump. The heart rhythm is coordinated by electrical action potentials that trigger Ca²⁺ signaling and cardiomyocyte contraction. The mechanical load during contraction can also feedback to affect the electrophysiology. Mechanical overload may lead to disruption of the action potential leading to arrhythmias. However, the mechanisms underlying mechano-electric coupling in cardiomyocytes remain unclear.
We developed the Patch-Clamp-in-Gel technology to investigate how the mechanical load on the cell affects the action potential and ion channels in the cardiomyocyte. Our data show that mechanical load prolonged action potential duration (APD), increased transient outward K⁺ current, decreased inward rectifier K⁺ current, and increased L-type Ca²⁺ current. Increased Ca²⁺ entry caused elevated SR Ca²⁺ load, increased cytosolic Ca²⁺ transient (CaT) and enhanced contractility. However, mechanical overload caused discordant alternans in APD and CaT which may lead to arrhythmias.