PDE1C inhibition or PDE1C silencing reduces SOCE in HASMCs.A, representative single-cell traces of changes in the fluorescence ratio (F/Fo) of fura-2 in control [vehicle, (DMSO, 0.01% v/v), black line] or C33 (1 μM)-treated (red line) HASMCs during ER(Ca2+) store depletion [0 Ca2+ + CPA (10 μM)] or during subsequent SOCE [2 mM Ca2+ + CPA (10 μM)]. B–E, impact of C33 on maximal [Ca2+] increases (B) and rate of increase (C) during ER(Ca2+) store depletions or maximal [Ca2+] increases (D) and rate of increase (E) during SOCE. Control n = 33, C33 n = 32 individual cells in which each treatment was analyzed. Student’s unpaired t test, ∗∗∗∗p < 0.0001 control versus C33 treated cells. F, representative single-cell traces of changes in the fluorescence ratio (F/Fo) of fura-2 in control siRNA transfected (black line) or PDE1C siRNA-transfected (red line) HASMCs during ER(Ca2+) store depletion [0 Ca2+ + CPA (10 μM)] or during subsequent SOCE [2 mM Ca2+ +CPA (10 μM)]. G–J, Impact of PDE1C-silencing on maximal [Ca2+] increases (G) and rate of increase (H) during ER(Ca2+) store depletions or maximal [Ca2+] increases (I) and rate of increase (J) during SOCE. siCtrl n = 35, siPDE1C n = 49 individual cells in which treatment was analyzed. Student’s unpaired t test, ∗p = 0.0340 siCtrl versus siPDE1C transfected cells. CPA, cyclopiazonic acid; HASMC, human arterial smooth muscle cell; PDE, phosphodiesterase; PDE1C, phosphodiesterase 1C; SOCE, store-operated calcium entry.