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首页> 外文期刊>American Journal of Physiology >A beta-peptides enhance vasoconstriction in cerebral circulation.
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A beta-peptides enhance vasoconstriction in cerebral circulation.

机译：β肽增强脑循环中的血管收缩。

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摘要

Amyloid-beta (A beta)-peptides are involved in the pathophysiology of Alzheimer's dementia. We studied the effects of A beta on selected constrictor responses of cerebral circulation. Mice were anesthetized (by using urethane-chloralose) and equipped with a cranial window. Arterial pressure and blood gases were monitored and controlled. Cerebral blood flow (CBF) was monitored by a laser Doppler probe. Topical superfusion with A beta 1-40 (0.1-10 microM), but not with the reverse peptide A beta 40-1, reduced resting CBF (-29 +/- 4% at 5 microM; P < 0.05) and augmented the reduction in CBF produced by the thromboxane analog U-46619 (+45 +/- 3% at 5 microM; P < 0.05). A beta 1-40 or A beta 1-42 did not affect the reduction in CBF produced by hypocapnia. The reduction in resting CBF and the enhancement of vasoconstriction were reversed by treatment with the free radical scavengers superoxide dismutase or manganic(I-II)meso-tetrakis(4-benzoic acid)porphyrin. Substitution of the methionine residue in position 35 with norleucine, a mutation that abolishes the ability of A beta to produce free radicals, abolished its vascular effects. Nanomolar concentrations of A beta 1-40 constricted isolated pressurized middle cerebral artery segments with intrinsic tone (-16 +/- 3% at 100 nM; P < 0.05). We conclude that A beta acts directly on cerebral arteries to produce vasoconstriction and to enhance selected constrictor responses. The evidence supports the idea that A beta-induced production of reactive oxygen species plays a role in this effect. The vascular actions of A beta may contribute to the deleterious effects resulting from accumulation of this peptide in Alzheimer's dementia.
机译：淀粉样β（A beta）肽参与阿尔茨海默氏痴呆症的病理生理。我们研究了A beta对选定的脑循环收缩反应的影响。麻醉小鼠（通过使用氨基甲酸酯-氯醛糖）并配备颅窗。监测和控制动脉压和血气。用激光多普勒探针监测脑血流量（CBF）。使用A beta 1-40（0.1-10 microM）进行局部灌注，但不使用反向肽A beta 40-1进行局部灌注，减少静息CBF（5 microM时为-29 +/- 4％; P <0.05），并增加减少量血栓烷类似物U-46619（在5 microM时+45 +/- 3％; P <0.05）产生的脑血流中的CSF。 β1-40或Aβ1-42不会影响低碳酸血症引起的CBF降低。通过用自由基清除剂超氧化物歧化酶或锰（I-II）间-四（4-苯甲酸）卟啉处理可以逆转静息CBF的降低和血管收缩的增强。正亮氨酸取代了35位的蛋氨酸残基，这种突变消除了A beta产生自由基的能力，从而消除了其血管效应。纳摩尔浓度的A beta 1-40压缩了具有固有音调的分离的加压大脑中动脉节段（在100 nM时为-16 +/- 3％; P <0.05）。我们得出的结论是，Aβ直接作用于脑动脉以产生血管收缩并增强选定的收缩反应。证据支持这样一种想法，即Aβ诱导的活性氧物质的产生在这种作用中起作用。 Aβ的血管作用可能会导致这种肽在阿尔茨海默氏痴呆症中的积累而产生有害作用。

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