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[一氧化氮与血管平滑肌的内稳态]

[Nitric oxide and homeostasis of the smooth vascular muscle].

作者信息

Schini V B, Vanhoutte P M

机构信息

Center for Experimental Therapeutics, Baylor College of Medicine, Houston, Texas.

出版信息

Arch Mal Coeur Vaiss. 1993 Jan;86 Spec No 1:83-9.

PMID:7692833
Abstract

Nitric oxide is synthesised from an amino acid, L-arginine, by a family of enzymes called nitric oxide (NO) synthase, by most cells in the vessel wall. In healthy vessels, the production of NO is due to the constitutive and calcium dependent NO synthase present in the endothelial cells. On the other hand, when the vascular system is diseased and defense mechanisms are activated, the mediators of inflammatory and immunitary reactions induce an NO synthase non-responsive to calcium which produces large quantities of NO in most of the cells of the vessel wall. Nitric oxide is a liposoluble radical with a short half-life. It plays a central role in the regulation of the motricity and proliferation of blood vessels and in the interaction of the blood cells with the vessel wall. An inadequate production of nitric oxide could play a role in many vascular diseases such as hypertension, atherosclerosis, restenosis or vascular hyporeactivity associated with septicaemic shock.

摘要

一氧化氮由一种氨基酸L-精氨酸通过一氧化氮合酶家族合成,血管壁中的大多数细胞均可合成。在健康血管中,一氧化氮的产生归因于内皮细胞中存在的组成型和钙依赖性一氧化氮合酶。另一方面,当血管系统患病且防御机制被激活时,炎症和免疫反应的介质会诱导一种对钙不敏感的一氧化氮合酶,这种酶会在血管壁的大多数细胞中产生大量一氧化氮。一氧化氮是一种半衰期短的脂溶性自由基。它在血管运动性和增殖的调节以及血细胞与血管壁的相互作用中起着核心作用。一氧化氮产生不足可能在许多血管疾病中起作用,如高血压、动脉粥样硬化、再狭窄或与败血性休克相关的血管反应低下。

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