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一氧化氮和S-亚硝基-L-半胱氨酸作为猫脑血管中乙酰胆碱产生的内皮源性舒张因子。

Nitric oxide and S-nitroso-L-cysteine as endothelium-derived relaxing factors from acetylcholine in cerebral vessels in cats.

作者信息

Kukreja R C, Wei E P, Kontos H A, Bates J N

机构信息

Department of Medicine, Medical College of Virginia, Richmond 23298.

出版信息

Stroke. 1993 Dec;24(12):2010-4; discussion 2014-5. doi: 10.1161/01.str.24.12.2010.

DOI:10.1161/01.str.24.12.2010
PMID:8248984
Abstract

BACKGROUND AND PURPOSE

The predominant view is that the endothelium-derived relaxing factor generated by acetylcholine from blood vessels is nitric oxide. However, there is evidence suggesting that certain nitric oxide-containing compounds such as nitrosothiols resemble the endothelium-derived relaxing factor generated by acetylcholine more closely than does nitric oxide itself. Accordingly, we compared the effects of nitric oxide and S-nitroso-L-cysteine on cerebral arteriolar caliber in relation to the associated increments in nitrite concentration in the effluent.

METHODS

Acetylcholine, nitric oxide, and S-nitroso-L-cysteine were administered by continuous superfusion in oxygen-free solution through the space under a cranial window in anesthetized cats. Nitrite concentration was measured in the effluent. The degree of vasodilation induced was evaluated in relation to the increment in nitrite concentration.

RESULTS

All agents induced dose-dependent vasodilation and dose-dependent increments in nitrite concentration in the effluent. For any given degree of vasodilation, the increments in nitrite concentration were equivalent during acetylcholine or S-nitroso-L-cysteine infusion, whereas the nitrite concentrations were 10 times higher during nitric oxide infusion. After administration of nitroarginine, a competitive inhibitor of nitric oxide synthesis from arginine, there was depression in the vasodilation as well as the increment in nitrite concentration induced by acetylcholine.

CONCLUSIONS

S-Nitroso-L-cysteine resembles endothelium-derived relaxing factor from acetylcholine more closely than does nitric oxide.

摘要

背景与目的

主流观点认为,血管中乙酰胆碱产生的内皮源性舒张因子是一氧化氮。然而,有证据表明,某些含一氧化氮的化合物,如亚硝基硫醇,比一氧化氮本身更类似于乙酰胆碱产生的内皮源性舒张因子。因此,我们比较了一氧化氮和S-亚硝基-L-半胱氨酸对脑动脉口径的影响以及流出液中亚硝酸盐浓度的相应增加。

方法

在麻醉猫的颅窗下间隙,通过在无氧溶液中持续灌注乙酰胆碱、一氧化氮和S-亚硝基-L-半胱氨酸。测量流出液中的亚硝酸盐浓度。根据亚硝酸盐浓度的增加评估诱导的血管舒张程度。

结果

所有药物均诱导剂量依赖性血管舒张和流出液中亚硝酸盐浓度的剂量依赖性增加。对于任何给定程度的血管舒张,乙酰胆碱或S-亚硝基-L-半胱氨酸输注期间亚硝酸盐浓度的增加是等效的,而一氧化氮输注期间亚硝酸盐浓度高10倍。给予硝基精氨酸(一种从精氨酸合成一氧化氮的竞争性抑制剂)后,乙酰胆碱诱导的血管舒张以及亚硝酸盐浓度的增加均受到抑制。

结论

S-亚硝基-L-半胱氨酸比一氧化氮更类似于乙酰胆碱产生的内皮源性舒张因子。

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Nitric oxide and S-nitroso-L-cysteine as endothelium-derived relaxing factors from acetylcholine in cerebral vessels in cats.一氧化氮和S-亚硝基-L-半胱氨酸作为猫脑血管中乙酰胆碱产生的内皮源性舒张因子。
Stroke. 1993 Dec;24(12):2010-4; discussion 2014-5. doi: 10.1161/01.str.24.12.2010.
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Effects in cats of inhibition of nitric oxide synthesis on cerebral vasodilation and endothelium-derived relaxing factor from acetylcholine.一氧化氮合成抑制对猫脑血流舒张及乙酰胆碱来源的内皮源性舒张因子的影响。
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NO forms an adduct with serum albumin that has endothelium-derived relaxing factor-like properties.
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Blockade of voltage-sensitive Ca(2+)-channels markedly diminishes nitric oxide- but not L-S-nitrosocysteine- or endothelium-dependent vasodilation in vivo.在体内,对电压敏感性钙通道的阻断显著减弱了一氧化氮介导的血管舒张,但对L-S-亚硝基半胱氨酸或内皮依赖性血管舒张没有影响。
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Endothelium-dependent relaxation to acetylcholine in bovine oviductal arteries: mediation by nitric oxide and changes in apamin-sensitive K+ conductance.牛输卵管动脉对乙酰胆碱的内皮依赖性舒张:一氧化氮的介导作用及阿帕明敏感钾离子通道电导的变化
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Vasorelaxant properties of the endothelium-derived relaxing factor more closely resemble S-nitrosocysteine than nitric oxide.内皮源性舒张因子的血管舒张特性更类似于S-亚硝基半胱氨酸而非一氧化氮。
Nature. 1990 May 10;345(6271):161-3. doi: 10.1038/345161a0.
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Independent blockade of cerebral vasodilation from acetylcholine and nitric oxide.乙酰胆碱和一氧化氮对脑血管舒张作用的独立阻断。
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The vasodilator potency of the endothelium-derived relaxing factor, L-S-nitrosocysteine, is impaired in conscious spontaneously hypertensive rats.内皮源性舒张因子L-S-亚硝基半胱氨酸的血管舒张效能在清醒自发性高血压大鼠中受损。
Vascul Pharmacol. 2006 Jun;44(6):476-90. doi: 10.1016/j.vph.2006.03.013. Epub 2006 May 11.
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Role of the L-arginine-nitric oxide pathway in the changes in cerebrovascular reactivity following hemorrhagic hypotension and retransfusion.
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