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遗传性高血压中的一氧化氮合酶活性

Nitric oxide synthase activity in genetic hypertension.

作者信息

Malinski T, Kapturczak M, Dayharsh J, Bohr D

机构信息

Department of Chemistry, Oakland University, Rochester, MI 48309-4401.

出版信息

Biochem Biophys Res Commun. 1993 Jul 30;194(2):654-8. doi: 10.1006/bbrc.1993.1871.

Abstract

A porphyrinic sensor was used to monitor nitric oxide released from cultured endothelial and vascular smooth muscle cells obtained from genetically hypertensive rats and from a normotensive reference strain of rats. Endothelial cell nitric oxide synthase (the constitutive enzyme) was stimulated with bradykinin, and vascular smooth muscle cell nitric oxide synthase (the inducible enzyme) was induced with interleukin-1 beta. Both types of cells from hypertensive rats released less nitric oxide than did cells from normotensive rats. The observed deficient nitric oxide release from endothelial and smooth muscle cells may contribute to the elevated vascular tone and increased cell growth described in hypertension.

摘要

使用一种卟啉传感器来监测从遗传性高血压大鼠以及正常血压对照品系大鼠获取的培养内皮细胞和血管平滑肌细胞释放的一氧化氮。用缓激肽刺激内皮细胞一氧化氮合酶(组成型酶),并用白细胞介素-1β诱导血管平滑肌细胞一氧化氮合酶(诱导型酶)。高血压大鼠的这两种细胞释放的一氧化氮均少于正常血压大鼠的细胞。观察到的内皮细胞和平滑肌细胞一氧化氮释放不足可能导致高血压中所述的血管张力升高和细胞生长增加。

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