AKAP150 is required for AngII-induced, PKC-dependent regulation of TRPV4 sparklet activity in arterial myocytes. (A) Representative records of [Ca2+]i from a TRPV4 sparklet site before (top) and after (bottom) application of 100 nM GSK in an AKAP150−/− arterial myocyte. The broken red lines show the amplitude of elementary TRPV4 sparklets. Solid red lines highlight basal [Ca2+]i. (B) Scatter plot of the activities of TRPV4 sparklet sites under control conditions and after application of GSK in WT (n = 10) and AKAP150−/− (n = 25) arterial myocytes. The red lines are the median values (*, P < 0.05; Mann-Whitney test). (C) Bar plot of the normalized (TRPV4/β-actin) TRPV4 transcript level in WT and AKAP150−/− myocytes (n = 3). Data are means ± SEM (error bars). ns, not significant. (D) TRPV4 sparklet records from an AKAP150−/− myocyte before and after application of 100 nM AngII. (E) Scatter plot of TRPV4 sparklet activities in WT (n = 23) and AKAP150−/− (n = 13) myocytes in the absence (control) and presence of AngII. The red lines are the median values (*, P < 0.05; Mann-Whitney test). (F) Histogram of the amplitudes of TRPV4 sparklets before and after exposing AKAP150−/− arterial myocytes to GSK. The red line is the best fit to the GSK data with a Gaussian function using a q value of 48 nM.