Effect of azelnidipine and amlodipine on single cell mechanics in mouse cardiomyocytes

Iribe, Gentaro; Kaihara, Keiko; Ito, Hiroshi; Naruse, Keiji

doi:10.1016/j.ejphar.2013.05.030

Cited by 10 publications

(6 citation statements)

References 22 publications

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“…In our previous report, the conventional stretch method allowed 5 to 8% stretch, approximately up to 2.0 m in SL (Iribe et al, 2013(Iribe et al, , 2009(Iribe et al, , 2007. On the other hand, the present improved cell gripping method allowed more than 15% stretch, approximately up to Lmax.…”

Section: New Gripping Systemmentioning

confidence: 99%

“…Ventricular myocytes were enzymatically isolated from hearts excised from C57BL/6 mice (aged 9-11 weeks), which were killed by cervical dislocation. The detailed cell isolation method is described elsewhere (Iribe et al, 2013). Isolated cells were stored in normal tyrode solution (140 mM NaCl, 5.4 mM KCl, 1.8 mM CaCl2, 1 mM MgCl2, 5 mM HEPES, 11 mM glucose, pH of 7.4 adjusted using NaOH).…”

Section: Myocyte Preparationmentioning

confidence: 99%

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Load dependency in force–length relations in isolated single cardiomyocytes

Iribe

Kaneko

Yamaguchi

et al. 2014

Progress in Biophysics and Molecular Biology

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The previously reported pressure-volume (PV) relationship in frog hearts shows that end-systolic PV relation (ESPVR) is load dependent, whereas ESPVR in canine hearts is load independent. To study intrinsic cardiac mechanics in detail, it is desirable to study mechanics in a single isolated cardiomyocyte that is free from interstitial connective tissue. Previous single cell mechanics studies used a pair of carbon fibers (CF) attached to the upper surface of opposite cell ends to stretch cells. These studies showed that end-systolic force-length (FL) relation (ESFLR) is load independent. However, the range of applicable mechanical load using the conventional technique is limited because of weak cell-CF attachment. Therefore, the behavior of ESFLR in single cells under physiologically possible conditions of greater load is not yet well known. To cover wider loading range, we contrived a new method to hold cell-ends more firmly using two pairs of CF attached to both upper and bottom surfaces of cells. The new method allowed stretching cells to 2.2 m or more in end-diastolic sarcomere length. ESFLR virtually behaves in a load independent manner only with end-diastolic sarcomere length less than 1.95 m. It exhibited clear load dependency with higher preload, especially with low afterload conditions. Instantaneous cellular elastance curves showed that decreasing afterload enhanced relaxation and slowed time to peak elastance, as previously reported. A simulation study of a mathematical model with detailed description of thin filament activation suggested that velocity dependent thin filament inactivation is crucial for the observed load dependent behaviors and previously reported afterload dependent change in Ca 2+ transient shape.

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Section: New Gripping Systemmentioning

confidence: 99%

Section: Myocyte Preparationmentioning

confidence: 99%

Load dependency in force–length relations in isolated single cardiomyocytes

Iribe

Kaneko

Yamaguchi

et al. 2014

Progress in Biophysics and Molecular Biology

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“…Ventricular myocytes were isolated from mice as previously described (Iribe et al, 2013(Iribe et al, , 2014. Mice (male C57BL/6J, 8-12 weeks old) were administered an intraperitoneal injection of heparin sodium (100 I.U.…”

Section: Ventricular Myocyte Isolationmentioning

confidence: 99%

Ischemia Enhances the Acute Stretch-Induced Increase in Calcium Spark Rate in Ventricular Myocytes

et al. 2020

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In ventricular myocytes, spontaneous release of calcium (Ca 2+) from the sarcoplasmic reticulum via ryanodine receptors ("Ca 2+ sparks") is acutely increased by stretch, due to a stretch-induced increase of reactive oxygen species (ROS). In acute regional ischemia there is stretch of ischemic tissue, along with an increase in Ca 2+ spark rate and ROS production, each of which has been implicated in arrhythmogenesis. Yet, whether there is an impact of ischemia on the stretch-induced increase in Ca 2+ sparks and ROS has not been investigated. We hypothesized that ischemia would enhance the increase of Ca 2+ sparks and ROS that occurs with stretch. Methods: Isolated ventricular myocytes from mice (male, C57BL/6J) were loaded with fluorescent dye to detect Ca 2+ sparks (4.6 µM Fluo-4, 10 min) or ROS (1 µM DCF, 20 min), exposed to normal Tyrode (NT) or simulated ischemia (SI) solution (hyperkalemia [15 mM potassium], acidosis [6.5 pH], and metabolic inhibition [1 mM sodium cyanide, 20 mM 2-deoxyglucose]), and subjected to sustained stretch by the carbon fiber technique (∼10% increase in sarcomere length, 15 s). Ca 2+ spark rate and rate of ROS production were measured by confocal microscopy. Results: Baseline Ca 2+ spark rate was greater in SI (2.54 ± 0.11 sparks•s −1 •100 µm −2 ; n = 103 cells, N = 10 mice) than NT (0.29 ± 0.05 sparks•s −1 •100 µm −2 ; n = 33 cells, N = 9 mice; p < 0.0001). Stretch resulted in an acute increase in Ca 2+ spark rate in both SI (3.03 ± 0.13 sparks•s −1 •100 µm −2 ; p < 0.0001) and NT (0.49 ± 0.07 sparks•s −1 •100 µm −2 ; p < 0.0001), with the increase in SI being greater than NT (+0.49 ± 0.04 vs. +0.20 ± 0.04 sparks•s −1 •100 µm −2 ; p < 0.0001). Baseline rate of ROS production was also greater in SI (1.01 ± 0.01 normalized slope; n = 11, N = 8 mice) than NT (0.98 ± 0.01 normalized slope; n = 12, N = 4 mice; p < 0.05), but there was an acute increase with stretch only in SI (+12.5 ± 2.6%; p < 0.001). Conclusion: Ischemia enhances the stretch-induced increase of Ca 2+ sparks in ventricular myocytes, with an associated enhancement of stretch-induced ROS production. This effect may be important for premature excitation and/or in the development of an arrhythmogenic substrate in acute regional ischemia.

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“…2 a) to measure tension and electrophysiological activity (Fig. 2 b) (Iribe et al 2013 ). Additionally, we recently developed a new stretching method that allows expansion of the myocardia up to the physiological sarcomere length experienced in the heart (Fig.…”

Section: Mechanosensorsmentioning

confidence: 99%

Mechanomedicine

Naruse

2018

Biophys Rev

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It has been a long time since the term mechanobiology became widely accepted, and broad research approaches, ranging from basic biology to medical research, have been conducted from the perspective of mechanobiology. Our group created the term “mechanomedicine” focusing on the field encompassing studies of the pathology and treatment of various diseases based on the knowledge obtained from mechanobiological studies and have promoted studies in this field. In the respiratory and cardiovascular systems, not only humoral factors but also physical factors such as contraction and expansion phenomena, and feedback from such phenomena to tissues and cells are important stimuli for maintaining homeostasis. Loss of homeostasis is considered to lead to pathological conditions. This review aims to provide an overview of mechanomedicine by introducing several mechanosensitive channels including one particular type of mechanosensor that we discovered in the cardiovascular system and by describing stretchable three-dimensional cell culture scaffolds using self-assembled peptides, a highly motile sperm sorter using a sperm sorting technique based on microfluidic mechanics, and a device to promote the development of fertilized ova.

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Effect of azelnidipine and amlodipine on single cell mechanics in mouse cardiomyocytes

Cited by 10 publications

References 22 publications

Load dependency in force–length relations in isolated single cardiomyocytes

Load dependency in force–length relations in isolated single cardiomyocytes

Ischemia Enhances the Acute Stretch-Induced Increase in Calcium Spark Rate in Ventricular Myocytes

Mechanomedicine

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