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.