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. Author manuscript; available in PMC: 2011 Apr 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2010 Jan 7;30(4):694–701. doi: 10.1161/ATVBAHA.109.200741

Figure 3. Csrp1-null smooth muscle displays a normal contractile response to phenylephrine or KCl.

Figure 3

(A) Dose response curve of the isometric contractile force in response to phenylephrine, a α 1 adrenergic agonist. Values were normalized based on the maximal force generation at the highest concentration. WT: wild type; Endo: presence (+) or absence (−) of endothelium. Note that no differences were detected between wild type and Csrp1−/− genotypes regardless of the presence of endothelium (repeated measures ANOVA, p>0.5). (B) Responses to KCl, which induce smooth muscle contraction by membrane depolarization, were also unaltered by the loss of CRP1. (C) Maximal isometric force development was compared in the absolute, and no statistical differences were detected (ANOVA, p>0.5). (D) Dose response curve of the isometric contractile force in response to KCl, assessed for bladder tissue. No difference was detected between the two genotypes (repeated measures ANOVA, p>0.5).