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Fig. 4 | The Journal of Physiological Sciences

Fig. 4

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

Fig. 4

Effects of pharmacological inhibition of the AT1R/TRPC3 pathway on the [Ca2+] transient in cardiomyocytes from C57BL/6 J mice in the stretch and angiotensin II (Ang II) protocols. a The significant slow increase in [Ca2+] transient at 300 s after the stretch (SSC) was suppressed by the inhibitors olmesartan (AT1R blocker, 10 μM; n = 10), U-73122 (PLC inhibitor, 10 μM; n = 9), BTP-2 (TRPC channels inhibitor, 10 μM; n = 9), and Pyr3 (TRPC3 inhibitor, 1 μM; n = 8). These inhibitors did not affect [Ca2+] transient at initial state and 10 s after the stretch. b The SSC-like significant increase in [Ca2+] transient induced by the application of Ang II for 300 s was suppressed by U-73122 (10 μM; n = 6), BTP-2 (10 μM; n = 12), and Pyr3 (1 μM; n = 8). These inhibitors did not affect [Ca2+] transient at initial state and 10 s after Ang II application. AT1R angiotensin II type 1 receptor, PLC phospholipase C, TRPC3 transient receptor potential canonical subtype 3

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