Increasing PKCα availability evokes TRPV4 channel activity in mesenteric myocytes. (A) TIRF image of a representative male mesenteric myocyte dialyzed with active PKCα (1 U/ml) recorded 1–5 min after gaining access to the cell interior. (B) Spatially averaged [Ca²⁺]_i from a myocyte dialyzed with active PKCα in the presence of the L-type Ca_V1.2 channel antagonist nifedipine (10 µM). (C) TRPV4 current records obtained using the whole-cell patch-clamp configuration. TRPV4 currents were defined as the fraction of the current sensitive to HC067047 (1 µM; control) and were obtained by subtracting current traces evoked by voltage ramps in the presence of HC067047 from traces in control conditions or in the presence of 100 nM AngII. (D) Bar plot showing mean ± SEM fold increase in I_TRPV4 at −80 mV in the presence (n = 7 cells) and absence (n = 7 cells) of active PKCα in the pipette solution. *, P < 0.05.