(Stroke. 2000;31:751.)
© 2000 American Heart Association, Inc.
Original Contributions |
Electromechanical Alterations in the Cerebrovasculature of Stroke-Prone Rats
From the Division of Basic Medical Sciences, Memorial University, St John’s, Newfoundland, Canada.
Background and Purpose—Cerebrovascular pressure-dependent constriction (PDC) is associated with smooth muscle (SM) depolarization and Ca2+ influx through voltage-gated channels. We studied the alterations in electromechanical contraction in the middle cerebral arteries (MCAs) of stroke-prone Wistar-Kyoto spontaneously hypertensive rats (SHRsp) in relation to the stroke-related loss of PDC.
Methods—Constriction to pressure, elevated [K+]o and/or [Ca2+]o, and SM membrane potentials (Em) were measured in isolated pressurized MCAs of SHRsp and stroke-resistant SHR.
Results—MCAs of SHRsp exhibited an age-related decrease in PDC before hemorrhagic stroke and a loss of PDC after stroke. At 100 mm Hg, the MCAs of poststroke SHRsp maintained partial constriction that was not altered with pressure but was inhibited by nifedipine (1 µmol/L). The MCAs of poststroke SHRsp constricted to vasopressin (0.17 µmol/L) but not to elevated [K+]o. When pressure was reduced from 100 to 0 mm Hg, the MCAs from young prestroke SHRsp exhibited SM hyperpolarization (-38 to -46 mV), whereas those of poststroke SHRsp maintained a constant, depolarized Em (-34 mV). Alterations in Em with varying [K+]o suggested that there was a decrease in SM K+ conductance in the MCAs of poststroke SHRsp.
Conclusions—The observation that the MCAs of poststroke SHRsp depolarize but do not constrict to elevated [K+]o suggests the presence of dysfunctional voltage-gated Ca2+ channels. The inability to alter Em with pressure or to constrict to depolarization could partially contribute to the loss of PDC in the MCAs of poststroke SHRsp.
Editorial Comment
Department of Obstetrics/Gynecology, University of Vermont, College of Medicine, Burlington, Vermont
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