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- W2883304290 abstract "Increased production of reactive oxygen species (ROS) has been linked to the pathogenesis of several cardiovascular diseases. However, it is largely unknown if ROS can regulate physiological cellular processes in the myocardium. The objective of the present study was to characterize the involvement of ROS in the positive inotropic effect of endothelin-1 (ET-1), the potential cellular sources of ROS, and the candidate downstream effectors of ROS. In the isolated perfused, paced rat heart preparation, intracoronary infusion of ET-1 (1 nmol/L) for 10 min increased developed tension by 45±6% (n=8, P + (mitoK ATP ) channels, decreased the inotropic effect of ET-1 by 43% (n=5, P ATP channels, and mitochondria-derived ROS may activate ERK and enhance cardiac contractility." @default.
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- W2883304290 date "2006-10-31" @default.
- W2883304290 modified "2023-09-23" @default.
- W2883304290 title "Abstract 1619: Endothelin-1 Regulates Cardiac Contractility via a Mitochondrial ATP-Sensitive K+ Channel-Dependent Activation of Extracellular Signal-Regulated Kinase" @default.
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