Chronic exposure to interleukin 1β induces a delayed and reversible alteration in excitation–contraction coupling of cultured cardiomyocytes

摘要: While proinflammatory cytokines can depress cardiac contractility, the mechanism by which this occurs remains unclear. To clarify cellular effects of interleukin (IL)-1β, we assessed calcium homeostasis, and gene expression in cardiomyocytes exposed to cytokine. Neonatal rat were IL-1β presence or absence an inhibitor nitric oxide (NO) synthase. Videomicroscopy was used follow transients (Fura-2 fluorescence) amplitude contraction, both unstimulated after isoproterenol challenge. Gene Northern Western blot analyses. Both basal contractility (amplitude maximum speed contraction relaxation) decreased, respectively, ca. 60% (P≤0.05) 40% 3 days exposure. Contractile function returned control values when cells where cultured additional IL-1β. IL-1β-treated had reduced responses as evidenced a lack enhanced reduction cAMP production. decreased genes important regulation homeostasis (phospholamban, sarcoplasmic reticulum ATPase) at transcript protein level. Alterations contractile did not occur through NO-mediated pathways. These results support hypothesis that may play role dysfunction alterations homeostasis.