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(Stroke. 2003;34:1491.)
© 2003 American Heart Association, Inc.

Original Contributions

Stroke Development in Stroke-Prone Spontaneously Hypertensive Rats Alters the Ability of Cerebrovascular Muscle to Utilize Internal Ca²⁺ to Elicit Constriction

From the Division of Basic Medical Sciences, Memorial University, St John’s, Newfoundland, Canada.

Correspondence to Dr J.S. Smeda, Division of Basic Medical Sciences, Room H4354, Memorial University, Health Science Center, St John’s, Newfoundland, Canada A1B 3V6. E-mail jsmeda{at}mun.ca

Background and Purpose— The ability of middle cerebral arteries (MCAs) to utilize intracellular smooth muscle (SM) Ca²⁺ to produce constriction in response to pressure and agonists was assessed in relation to hemorrhagic stroke development in Wistar-Kyoto stroke-prone (SHRSP) and stroke-resistant (srSHR) spontaneously hypertensive rats.

Methods— MCAs were studied with the use of a pressure myograph at 100 mm Hg.

Results— MCAs from srSHR and prestroke SHRSP exhibited pressure-dependent constriction and constricted in response to vasopressin or serotonin in the presence of nifedipine or the absence of [Ca²⁺]_o. MCAs from poststroke SHRSP lost the latter functions and could only constrict in response to vasopressin/serotonin in Krebs’ solution containing Ca²⁺ in the absence of nifedipine. This indicated that the SM could not utilize internal Ca²⁺ for constriction and maintained constriction by Ca²⁺ entry through L-type channels. The MCAs of poststroke SHRSP could not constrict to [K⁺]_o-induced depolarization, suggesting that the agonist-induced opening of the L-type channels occurred by mechanisms other than SM depolarization. Depletion of the sarcoplasmic SM Ca²⁺ stores of MCAs from srSHR with cyclopiazonic acid did not prevent pressure-dependent constriction.

Conclusions— Stroke in SHRSP produced a defect in the ability of MCAs to constrict in response to vasopressin or serotonin via the use of an intracellular source of Ca²⁺. This could be promoted by an inability of the SM to release intracellular Ca²⁺, by the depletion of internal Ca²⁺ stores, or by a decrease in the contractile sensitivity to Ca²⁺ released from the internal stores.

Key Words: calcium • hypertension • muscle, smooth • sarcoplasmic reticulum • stroke • vasopressins