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

• DOI: 10.1007/s12576-016-0519-3
• Publication Date: 2017-01-19T21:40:00Z
• Authors: Yohei Yamaguchi; Gentaro Iribe; Toshiyuki Kaneko; Ken Takahashi; Takuro Numaga-Tomita; Motohiro Nishida; Lutz Birnbaumer; Keiji Naruse
• Keywords: TRPC3; TRPC6

When a cardiac muscle is held in stretched position, its [Ca2+] transient increases slowly over several minutes process known as stress-induced slow increase intracellular Ca2+ concentration ([Ca2+]i) (SSC). Transient receptor potential canonical (TRPC) 3 forms non-selective cation channel regulated by the angiotensin II type 1 (AT1R). In this study, we investigated role of TRPC3 SSC. Isolated mouse ventricular myocytes were electrically stimulated and subjected to sustained stretch. An AT1R blocker, phospholipase C inhibitor, inhibitor suppressed These inhibitors also abolished observed SSC-like [Ca2+]i induced II, instead Furthermore, SSC was not knockout mice. Simulation immunohistochemical studies suggest that sarcolemmal responsible for results indicate TRPC3, AT1R, causes