Figure 4.
Actin depolymerization reverses the inward remodelling caused by 4 h of exposure to NE + Ang-II. (A) Arterioles exposed (4 h) to NE (10−5.5 M) + Ang-II (10−7 M). Before and after the 4 h incubation with NE + Ang-II, arterioles were allowed to develop spontaneous myogenic tone, and were exposed to adenosine (Ado, 10−4 M), and then to calcium-free solution. After 5 min under the second exposure to calcium-free conditions, arterioles were treated (1 h) with vehicle control (n = 8), cytochalasin-D (10 μM, n = 9), or mycalolide-B (2 μM, n = 11). Data are means ± SE of the per cent maximal diameter obtained under calcium-free conditions before the 4 h incubation with NE + Ang-II. *P ≤ 0.05 vs. control or cytochalasin-D. (B) Change in diameter caused by exposure to vehicle control, cytochalasin-D, or mycalolide-B is expressed as a per cent change from the reduction in passive diameter following the second exposure to calcium-free conditions. Data are means ± SE. *P ≤ 0.05 vs. control or cytochalasin-D. (C) Three-dimensional reconstruction images of arterioles stained with DAPI (red) to visualize nuclei, phalloidin (green) to visualize F-actin, and in the left panel anti-tubulin antibody (blue) to visualize microtubules. Left, control vessels were incubated with vehicle control for 1 h. Middle, arterioles were exposed to 10 μM cytochalasin-D for 1 h. Right, arterioles were exposed (1 h) to 2 μM mycalolide-B and show an almost complete disruption of the actin cytoskeleton. Microtubules stained (blue) show that cytoskeletal structures other than F-actin remained intact.