TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca²⁺ concentration in mouse cardiomyocytes.

ABSTRACT: When a cardiac muscle is held in a stretched position, its [Ca²⁺] transient increases slowly over several minutes in a process known as stress-induced slow increase in intracellular Ca²⁺ concentration ([Ca²⁺]_i) (SSC). Transient receptor potential canonical (TRPC) 3 forms a non-selective cation channel regulated by the angiotensin II type 1 receptor (AT1R). In this study, we investigated the role of TRPC3 in the SSC. Isolated mouse ventricular myocytes were electrically stimulated and subjected to sustained stretch. An AT1R blocker, a phospholipase C inhibitor, and a TRPC3 inhibitor suppressed the SSC. These inhibitors also abolished the observed SSC-like slow increase in [Ca²⁺]_i induced by angiotensin II, instead of stretch.

SUBMITTER: Yamaguchi Y 

PROVIDER: S-EPMC10718017 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature