From the Department of Surgery, Division of Vascular Surgery, Oregon
Health Sciences University, Portland (M.J.C.) and Department of Obstetrics and
Gynecology, University of Vermont College of Medicine, Burlington (G.O.).
Correspondence to Marilyn J. Cipolla, PhD, Division of Vascular Surgery, OP-11, Oregon Health Sciences University, 3181 SW Sam Jackson Park Rd, Portland, OR 97201. E-mail cipollam{at}ohsu.edu
Background and Purpose—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.
Methods—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 µmol/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.
Results—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).
Conclusions—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.
Associate
Editor for Basic Science School of Medicine Medical
College of Virginia Richmond, Virginia
© 1998 American Heart Association, Inc.
Original Contributions
Vascular Smooth Muscle Actin Cytoskeleton in Cerebral Artery Forced Dilatation
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