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In diabetic ventricular myocytes, transient outward potassium current (Ito) amplitude is severely reduced because of the impaired catecholamine release that characterizes diabetic autonomic neuropathy. Sympathetic nervous system exhibits a trophic effect on Ito since incubation of myocytes with noradrenaline restores current amplitude via beta-adrenoceptor (βAR) stimulation. Here, we investigate the intracellular signalling pathway though which incubation of diabetic cardiomyocytes with the βAR agonist isoproterenol recovers Ito amplitude to normal values.

Mechanisms Responsible for the Trophic Effect of Beta-Adrenoceptors on the ItoCurrent Density in Type 1 Diabetic Rat Cardiomyocytes

Mechanisms Responsible for the Trophic Effect of Beta-Adrenoceptors on the I_toCurrent Density in Type 1 Diabetic Rat Cardiomyocytes