Channelpedia

PubMed 19744491


Referenced in Channelpedia wiki pages of: none

Automatically associated channels: KChip2a , Kv1.4 , Kv3.1 , Kv4.2 , Kv4.3



Title: Molecular and functional remodeling of I(to) by angiotensin II in the mouse left ventricle.

Authors: Magdalini Tozakidou, Diane Goltz, Till Hagenström, Mareike K Budack, Helga Vitzthum, Kamila Szlachta, Robert Bähring, Heimo Ehmke

Journal, date & volume: J. Mol. Cell. Cardiol., 2010 Jan , 48, 140-51

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/19744491


Abstract
The transient outward potassium current (I(to)) in cardiac myocytes is mainly mediated by members of the Kv4 subfamily of voltage-gated potassium channels. Several in vitro studies have shown that angiotensin II (Ang II), which plays an important role in the development of cardiac hypertrophy, rapidly downregulates Kv4.3 mRNA expression. However, it is not clear whether Ang II regulates I(to)in vivo and whether this regulation may depend on alterations in Kv4.3 gene expression. To address this question, we determined the effects of acute (24 h) and chronic (14 days) exogenous infusions of Ang II on I(to) and the expression of its channel subunits in the mouse left ventricle. Ang II rapidly increased blood pressure and reduced Kv4.2 but not Kv4.3 mRNA levels in the absence of cardiac hypertrophy. In response to chronically elevated Ang II levels cardiac hypertrophy developed, which was associated with a downregulation of Kv4.2 and Kv4.3 mRNA levels, and an upregulation of Kv1.4 mRNA levels. In contrast, neither KChIP2 mRNA levels nor amplitude or macroscopic inactivation kinetics of I(to) were affected by the acute or chronic Ang II treatments. Consistent with the unchanged I(to) amplitude, Kv4.2, Kv4.3, and KChIP protein expression levels were similar after chronic Ang II and sham treatment. Our findings demonstrate that elevations of Ang II concentrations that induce hypertension and cardiac hypertrophy do not alter the amplitude of I(to) in the mouse left ventricle. Furthermore, they suggest that functional expression of cardiac I(to) in mice is stabilized by KChIP2.