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Articles in PresS, published online ahead of print December 20, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00441.2001
Submitted on May 24, 2001
Accepted on December 13, 2001
1 Obstetrics and Gynecology, University of Vermont, Burlington, Vermont, USA
* To whom correspondence should be addressed. E-mail: gokina{at}salus.med.uvm.edu.
The objective of this study was to examine the role of the actin cytoskeleton in the development of pressure-induced membrane depolarization and calcium influx underlying myogenic constriction in cerebral arteries. Elevating intraluminal pressure from 10 to 60 mmHg induced membrane depolarization, increased [Ca2+]i and elicited myogenic constriction in both intact and denuded rat posterior cerebral arteries. Pretreatment with cytochalasin D (5 µM) or latrunculin A (3µM) abolished constriction but enhanced the [Ca2+]i response; similarly, acute application of cytochalasin D to vessels with tone, or in the presence of 60 mM K+, elicited relaxation accompanied by an increase [Ca2+]i. The effects of cytochalasin D were inhibited by nifedipine (3 µM), demonstrating that actin cytoskeletal disruption augments Ca2+ influx through voltage-sensitive L-type Ca2+ channels. Finally, pressure-induced depolarization was enhanced in the presence of cytochalasin D, further substantiating a role for the actin cytoskeleton in the modulation of ion channel function. Together, these results implicate the VSM actin cytoskeleton in the control of cerebral artery diameter through its influence on membrane potential, as well as via a direct inhibitory effect on L-type Ca2+ channels.
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