High Hydrostatic Pressure induces Cardiomyocyte Contraction

抄録

Cardiac muscles are subject to several types of mechanical stress. The mechanical stress affects the morphological and functional aspects of cardiomyocytes. However, the effect of high-pressure in cardiomyocytes has never been investigated due to the lack of a quantitative measurement system. In this study, we first successfully observed the alteration of the morphology and intracellular Ca²⁺ concentration ([Ca²⁺]_i) in mouse cardiomyocytes under high-hydrostatic pressure. The high-pressures (5, 10, and 20 MPa) progressively shortened the sarcomere length as an index of morphological change with the high-hydrostatic pressure system. However, electron microscope indicated that the high pressure did not collapse the organisation of cardiomyocytes. In the high-pressure microscope, high-pressure did not change [Ca²⁺]_i, though the cardiomyocyte contracted. Furthermore, 50 mM 2,3-Butanedione monoxime, a non-selective myosin ATPase inhibitor, interrupted the high-pressure-induced contraction in cardiomyocytes . These results suggest that high hydrostatic pressure directly regulates actomyosin interaction, leading to the cardiomyocyte contraction.