Vascular smooth muscle actin cytoskeleton in cerebral artery forced dilatation

We investigated the role of actin polymerization in regulating arterial diameter in response to increasing pressure and modulating forced dilatation of cerebral arteries at pressures above the upper limit of autoregulation.

Posterior cerebral arteries (n = 12) were isolated and pressurized in a special arteriograph that allowed control of intravascular pressure and measurement of lumen diameter. Intact arteries in the absence (control) or presence of 3.0 mumol/L cytochalasin B (CB), an inhibitor of actin polymerization, were subjected to stepwise increases in pressure from 75 to 200 mm Hg. Lumen diameter was continuously recorded, as was the pressure at which forced dilatation (loss of tone) occurred. After a period of time at 200 mm Hg, pressure was returned to 75 mm Hg and the extent of tone recovery was evaluated.

Arteries with and without CB developed a similar amount of tone during equilibration at 75 mm Hg: percent tone = 27 +/- 3% for control versus 29 +/- 4% for CB arteries (P > 0.05). However, arteries in the presence of CB could not withstand pressure as well and underwent FD at significantly lower pressures: 168 +/- 5 mm Hg for control versus 142 +/- 5 mm Hg for CB arteries (P < 0.01). The amount of tone that arteries regained after FD when pressure was returned to 75 mm Hg was also less in CB arteries: percent tone = 34 +/- 3% for control versus 11 +/- 2% for CB arteries (P < 0.01).

Cytoskeletal integrity appears important for maintaining cerebral arterial diameter during changing intravascular pressure. In addition, the process of actin polymerization may be a significant contributor to development of myogenic tone after forced dilatation.