Myocardial TRPC6-mediated Zn²⁺ influx induces beneficial positive inotropy through β-adrenoceptors.

ABSTRACT: Baroreflex control of cardiac contraction (positive inotropy) through sympathetic nerve activation is important for cardiocirculatory homeostasis. Transient receptor potential canonical subfamily (TRPC) channels are responsible for α₁-adrenoceptor (α₁AR)-stimulated cation entry and their upregulation is associated with pathological cardiac remodeling. Whether TRPC channels participate in physiological pump functions remains unclear. We demonstrate that TRPC6-specific Zn²⁺ influx potentiates β-adrenoceptor (βAR)-stimulated positive inotropy in rodent cardiomyocytes. Deletion of trpc6 impairs sympathetic nerve-activated positive inotropy but not chronotropy in mice. TRPC6-mediated Zn²⁺ influx boosts α₁AR-stimulated βAR/G_s-depe

SUBMITTER: Oda S 

PROVIDER: S-EPMC9606288 | biostudies-literature | 2022 Oct

REPOSITORIES: biostudies-literature