Activation of TRPV1 attenuates high salt-induced cardiac hypertrophy through improvement of mitochondrial function.

ABSTRACT:

Background and purpose

High-salt diet induces cardiac remodelling and leads to heart failure, which is closely related to cardiac mitochondrial dysfunction. Transient receptor potential (TRP) channels are implicated in the pathogenesis of cardiac dysfunction. We investigated whether activation of TRP vanilloid (subtype 1) (TRPV1) channels by dietary capsaicin can, by ameliorating cardiac mitochondrial dysfunction, prevent high-salt diet-induced cardiac hypertrophy.

Experimental approach

Male wild-type (WT) and TRPV1(-/-) mice were fed a normal or high-salt diet with or without capsaicin for 6 months. Their cardiac parameters and endurance capacity were assessed. Mitochondrial respiration and oxygen consumption were measured using high-resolution respirometry. The expression

SUBMITTER: Lang H 

PROVIDER: S-EPMC4667858 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature