抄録
Cardiomyocytes respond to a mechanical stretch with an intracellular calcium increase. Extensive stretch of the cardiomyocyte may induce pathological condition to the heart, such as arrhythmia. However, the molecular mechanism responsible for the mechanosensitivity of the cardiomyocyte is not fully understood. We have studied the role of the mechanosensitive ion channels, TRPCs and TRPV2, in the stretch-induced calcium response of the rat cardiomyocyte cell line H9c2. The cells were cultured on a flexible silicone chamber and were loaded with the calcium sensitive dye Fura2. The intracellular calcium concentration increased in proportion to the extent of the chamber stretch. This calcium response was completely blocked by a bath application of calcium free solution. Furthermore, neither 5 uM-thapsigargin nor 2 uM-ryanodine altered the stretch-induced calcium response, suggesting that the calcium increase is mainly caused by Ca2+ influx from external space probably via channel mechanism. Bath application of the TRPV2 channel blocker, ruthenium red (50 uM), inhibited the stretch-induced calcium increase by 70%. In contrast, the TRPC channel blockers, BTP2 (100 uM) and SKF-96365 (50 uM), showed no effect on the stretch-induced calcium response. These results suggest that the stretch-sensitivity of the rat cardiomyocyte H9c2 is attributable to the mechanosensitive ion channel TRPV2. [J Physiol Sci. 2008;58 Suppl:S177]
