Dataset Information

Different protein kinase C isoenzymes mediate inhibition of cardiac rapidly activating delayed rectifier K⁺ current by different G-protein coupled receptors.

ABSTRACT:

Background and purpose

Elevated angiotensin II (Ang II) and sympathetic activity contributes to a high risk of ventricular arrhythmias in heart disease. The rapidly activating delayed rectifier K⁺ current (I_Kr ) carried by the hERG channels plays a critical role in cardiac repolarization, and decreased I_Kr is involved in increased cardiac arrhythmogenicity. Stimulation of α_1A -adrenoreceptors or angiotensin II AT₁ receptors is known to inhibit I_Kr via PKC. Here, we have identified the PKC isoenzymes mediating the inhibition of I_Kr by activation of these two different GPCRs.

Experimental approach

The whole-cell patch-clamp technique was used to record I_Kr in guinea pig cardiomyocytes and H

SUBMITTER: Liu X

PROVIDER: S-EPMC5715974 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Dataset Information

Different protein kinase C isoenzymes mediate inhibition of cardiac rapidly activating delayed rectifier K⁺ current by different G-protein coupled receptors.

Background and purpose

Experimental approach

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

Different protein kinase C isoenzymes mediate inhibition of cardiac rapidly activating delayed rectifier K+ current by different G-protein coupled receptors.

Background and purpose

Experimental approach

OmicsDI is part of the ELIXIR infrastructure

Tweets

Different protein kinase C isoenzymes mediate inhibition of cardiac rapidly activating delayed rectifier K⁺ current by different G-protein coupled receptors.