Figure 9.

Loss of zyxin leads to a contractile deficit of VSMCs in vitro and isolated femoral arteries in situ. A, Analysis of the ability of WT and zyxin^−/− VSMCs to pull a collagen gel, thereby reducing its diameter over a time period of 24 hours, an indirect measure of the contractility of the VSMCs. VSMCs seeded in the collagen gels were additionally stimulated with vasoconstrictor agonists such as ET1, Eph, and NE (100 nmol/L of each agonist). *P<0.05, ***P<0.001 as indicated, n=4 for each experimental group. B, Pressure-diameter measurements of isolated femoral arteries from WT and zyxin^−/− mice in the absence and presence of increasing concentrations of vasoconstrictors, Eph and ET1; 10⁻⁸ to 10⁻⁶ mol/L. Acetylcholine was used as a control for vessel integrity indicated by vasodilatation. *P<0.05, **P<0.01, and ***P<0.001 as indicated, n=3 to 5. Mean values for vessel diameter from “n” individual experiments were compared between WT and zyxin^−/− mice at each data point by unpaired t test. Eph indicates epinephrine; ET1, endothelin 1; NE, norepinephrine; VSMCs, vascular smooth muscle cells; WT, wild type.