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Phosphatidylinositol 3‐kinase‐δ up‐regulates L‐type Ca 2+ currents and increases vascular contractility in a mouse model of type 1 diabetes
Author(s) -
Pinho JF,
Medeiros MAA,
Capettini LSA,
Rezende BA,
Campos PP,
Andrade SP,
Cortes SF,
Cruz JS,
Lemos VS
Publication year - 2010
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2010.00955.x
Subject(s) - contractility , endocrinology , medicine , pi3k/akt/mtor pathway , phenylephrine , vascular smooth muscle , phosphatidylinositol , vasoconstriction , chemistry , biology , kinase , microbiology and biotechnology , signal transduction , smooth muscle , blood pressure
Vasculopathies represent the main cause of morbidity and mortality in diabetes. Vascular malfunctioning in diabetes is associated with abnormal vasoconstriction and Ca(2+) handling by smooth muscle cells (SMC). Phosphatidylinositol 3-kinases (PI3K) are key mediators of insulin action and have been shown to modulate the function of voltage-dependent L-type Ca(2+) channels (Ca(V) 1.2). In the present work, we investigated the involvement of PI3K signalling in regulating Ca(2+) current through Ca(V) 1.2 (I(Ca,L) ) and vascular dysfunction in a mouse model of type I diabetes.