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Fig. 6. Ca²⁺-cycling in S100A1-treated NVCMs is regulated via PLC-PKC activation of NCX. (A) Inhibition of NCX activity by myr-FRCRCFa (30 µM) abrogated the S100A1-mediated decline in diastolic [Ca²⁺]_i in NVCMs. (B,C) The S100A1-mediated decrease in diastolic [Ca²⁺]_i is abolished trough inhibition of PLC and PK C by U-73122 and calphostin-c, respectively. ^*P<0.01 vs. control. Measurements represent n=50 cells from three independent cell preparations. Data are given as mean±s.e.m.

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