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

Raúl Setién | Zendy; Aintzane Alday | Zendy; Cristina Diaz-Asensio | Zendy; Janire Urrutia | Zendy; Mónica Gallego | Zendy; Óscar Casis | Zendy

Open Access

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

Author(s) -

Raúl Setién,

Aintzane Alday,

Cristina Diaz-Asensio,

Janire Urrutia,

Mónica Gallego,

Óscar Casis

Publication year - 2013

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000343346

Subject(s) - medicine , endocrinology , adenylyl cyclase , protein kinase a , stimulation , myocyte , cardiac transient outward potassium current , agonist , patch clamp , receptor , gs alpha subunit , chemistry , biology , microbiology and biotechnology , phosphorylation

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.

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