Fig. 9. Antisense knockdown of SmAV decreases contractility and signaling in smooth-muscle tissue. (A) Densitometric analysis of SmAV protein levels from immunoblots of antisense- and sham-treated muscles expressed as a precentage of random loaded tissue. ^**P0.01. (Inset) A typical western blot for SmAV. (B) Magnitude of steady-state contraction in response to a depolarizing physiological saline solution containing 51 mM KCl. Forces are normalized to the amplitude of contraction of each muscle in response to 51 mM KCl physiological saline solution on day 1. (C) Contraction of muscle strips in response to the phorbol ester DPBA (3 µM). Forces are normalized to the amplitude of contraction of each muscle in response to 51 mM KCl on day 1. ^**P0.01 for antisense compared with sham; ⁺⁺P0.001 for antisense compared with random. (D) Contraction of muscle strips in response to 10 µM phenylephrine in the absence of extracellular calcium. Forces are normalized to the amplitude of contraction of each muscle in response to 51 mM KCl physiological saline on day 1. ^*P0.05 for antisense compared with sham; ⁺P0.05 for antisense compared with random. (E) Densitometric analysis of phospho-ERK1/2 on immunoblots for antisense- or sham-treated muscles exposed to DPBA, normalized to that for muscles treated with a random sequence. (Inset) A typical western blot for phospho-ERK1/2. ^**P0.05. All values are from between three and five separate experiments.