Alpha1-adrenoceptor stimulation potentiates L-type Ca2+ current through Ca2+/calmodulin-dependent PK II (CaMKII) activation in rat ventricular myocytes.

ABSTRACT: alpha1-Adrenoceptor stimulation (alpha1ARS) modulates cardiac muscle contraction under physiological conditions by means of changes in Ca2+ current through L-type channels (ICa,L) and Ca2+ sensitivity of the myofilaments. However, the cellular mechanisms of alpha1ARS are not fully clarified. In this study, we investigated the role of Ca2+/calmodulin-dependent PK II (CaMKII) in the regulation of ICa,L during alpha1ARS in isolated adult rat ventricular myocytes by using the perforated patch-clamp technique. CaMKII inhibition with 0.5 microM KN-93 abolished the potentiation in ICa,L observed during alpha1ARS by 10 microM phenylephrine. In the presence of PKC inhibitor (10 microM chelerythrine), the potentiation of ICa,L by phenylephrine also disappeared. In Western immunoblotting analysis, ph

SUBMITTER: O-Uchi J 

PROVIDER: S-EPMC1166620 | biostudies-literature | 2005 Jun

REPOSITORIES: biostudies-literature