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Fig. 4. Inhibition of SR Ca²⁺-fluxes abolishes enhanced Ca²⁺-cycling in S100A1-overexpressing but not in S100A1-treated NVCMs. (A) Addition of the SERCA2a inhibitor thapsigargin (1 µM) abolishes the S100A1-induced increase in the Ca²⁺-transient amplitude in overexpressing (AdS100A1) but not S100A1-treated NVCMs. (B) Thapsigargin reduces diastolic [Ca²⁺]_i in control and S100A1-overexpressing cells, whereas S100A1-treated cells are not significantly affected. (C) SERCA2a inhibition raises the decay-constant ${tau}$ in control and AdS100A1-infected NVCMs but does not significantly alter ${tau}$ in S100A1-treated NVCMs. (D) Tetracaine (100 µM), an inhibitor of the SR Ca²⁺-release channel (RyR), abrogates the increased Ca²⁺-transient amplitude in S100A1-overexpressing NVCMs but does not significantly reduce the augmented amplitude of the Ca²⁺-transient in S100A1-treated NVCMs relative to tetracaine-treated control cells. ^*P<0.01 vs. control. Measurements represent n=150 cells from three independent cell preparations. Data are given as mean±s.e.m.

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