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Published on: June 14, 2015
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High hydrostatic pressure induces slow contraction in mouse cardiomyocytes
Yohei Yamaguchi1, Masayoshi Nishiyama2, Hiroaki Kai3
1Department of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan; Department of Physiology, Asahikawa Medical University, Asahikawa, Hokkaido, Japan.
Biophysical Journal
|July 16, 2022
Summary
High hydrostatic pressure causes slow cardiomyocyte contractions without a calcium increase. Myosin ATPase inhibition stops these pressure-induced contractions, revealing a novel mechanism.
Area of Science:
- Cardiovascular Physiology
- Cellular Mechanics
- Biophysics
Background:
- Cardiomyocytes are essential for heart contraction, with calcium flux regulating actomyosin interactions.
- Physical factors like hydrostatic pressure can modulate cardiomyocyte contractility.
- The precise mechanism of pressure-induced cardiomyocyte contraction remains unclear.
Purpose of the Study:
- To investigate the mechanism underlying slow cardiomyocyte contractions induced by high hydrostatic pressure.
- To characterize changes in cell morphology and intracellular calcium concentration ([Ca2+]i) under pressure.
Main Methods:
- Utilized a high-pressure microscope to observe mouse cardiomyocytes under elevated hydrostatic pressures.
- Measured intracellular calcium concentration ([Ca2+]i) and cell morphology.
- Employed transmission electron microscopy (TEM) and a myosin ATPase inhibitor.
Main Results:
- Cardiomyocytes exhibited slow contractions under high pressure without a transient increase in [Ca2+]i.
- A myosin ATPase inhibitor effectively blocked these pressure-induced slow contractions.
- TEM revealed sarcomere shortening at 20 MPa, but cellular structures remained intact.
Conclusions:
- Pressure-induced slow cardiomyocyte contractions are driven by actomyosin interactions.
- This process occurs independently of an acute transient increase in intracellular calcium.
- High hydrostatic pressure affects cardiomyocyte contractility through a calcium-independent pathway.
