Smeda J S, King S
Division of Basic Medical Sciences, Memorial University, St John's, Newfoundland, Canada.
Stroke. 2000 Mar;31(3):751-8; discussion 758-9. doi: 10.1161/01.str.31.3.751.
Cerebrovascular pressure-dependent constriction (PDC) is associated with smooth muscle (SM) depolarization and Ca(2+) 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.
Constriction to pressure, elevated K(+) and/or Ca(2+), and SM membrane potentials (E(m)) were measured in isolated pressurized MCAs of SHRsp and stroke-resistant SHR.
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 micromol/L). The MCAs of poststroke SHRsp constricted to vasopressin (0.17 micromol/L) but not to elevated K(+). 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 E(m) (-34 mV). Alterations in E(m) with varying K(+) suggested that there was a decrease in SM K(+) conductance in the MCAs of poststroke SHRsp.
The observation that the MCAs of poststroke SHRsp depolarize but do not constrict to elevated K(+) suggests the presence of dysfunctional voltage-gated Ca(2+) channels. The inability to alter E(m) with pressure or to constrict to depolarization could partially contribute to the loss of PDC in the MCAs of poststroke SHRsp.
脑血管压力依赖性收缩（PDC）与平滑肌（SM）去极化以及通过电压门控通道的Ca(2+)内流有关。我们研究了易中风的Wistar-Kyoto自发性高血压大鼠（SHRsp）大脑中动脉（MCA）的机电收缩变化与中风相关的PDC丧失之间的关系。
在分离的加压SHRsp和抗中风SHR的MCA中测量对压力、升高的K(+)和/或Ca(2+)的收缩以及SM膜电位（E(m)）。
SHRsp的MCA在出血性中风前表现出与年龄相关的PDC降低，中风后PDC丧失。在100 mmHg时，中风后SHRsp的MCA维持部分收缩，该收缩不随压力改变，但被硝苯地平（1 μmol/L）抑制。中风后SHRsp的MCA对血管加压素（0.17 μmol/L）收缩，但对升高的K(+)不收缩。当压力从100 mmHg降至0 mmHg时，年轻的中风前SHRsp的MCA表现出SM超极化（-38至-46 mV），而中风后SHRsp的MCA维持恒定的去极化E(m)（-34 mV）。随着K(+)变化的E(m)改变表明中风后SHRsp的MCA中SM K(+)电导降低。
中风后SHRsp的MCA去极化但对升高的K(+)不收缩的观察结果表明存在功能失调的电压门控Ca(2+)通道。无法随压力改变E(m)或对去极化收缩可能部分导致中风后SHRsp的MCA中PDC丧失。
