Ca⁺²/Calmodulin-Dependent Protein Kinase Mediates Glucose Toxicity-Induced Cardiomyocyte Contractile Dysfunction

Figure 6

Mechanical property of rat cardiomyocytes cultured for 12 hours in a serum-free medium with normal glucose (NG: 5.5 mM) or high glucose (HG: 25.5 mM) in the absence or presence of high or low extracellular Ca²⁺ (Hi-Ca = 2.7 mM; LoCa = 1.0 mM) in the recording contractile buffer. A cohort of HG-cultured cardiomyocytes was recorded in high Ca²⁺ environment in the presence of the CaM kinase inhibitor KN93 (10 μM). (a) Resting cell length, (b) peak shortening (PS) amplitude normalized to cell length, (c) maximal velocity of shortening (+dL/dt), (d) maximal velocity of relengthening (−dL/dt), (e) time to PS (TPS), and (f) time to 90% relengthening (TR₉₀). Mean ± SEM, 𝑛=10 cells per group, *𝑃<0.05 versus NG-LoCa group, ^#𝑃<0.05 versus HG-LoCa group, ^†𝑃<0.05 versus NG-HCa-KN93 group.

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