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.