Upregulation of vascular NAD(P)H oxidase subunit gp91phox and impairment of the nitric oxide signal transduction pathway in hypertension

被引：56

作者：

Morawietz, H

Weber, M

Rueckschloss, U

Lauer, N

Hacker, A

Kojda, G

机构：

[1] Univ Dusseldorf, Inst Pharmakol, D-40225 Dusseldorf, Germany

[2] Univ Dusseldorf, Klin Pharmakol, D-40225 Dusseldorf, Germany

[3] Univ Halle Wittenberg, Inst Pathophysiol, D-4020 Halle An Der Saale, Germany

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2001年 / 285卷 / 05期

关键词：

hypertension; NADPH oxidase; superoxide; nitric oxide; guanylate cyclase; signal transduction; endothelial function;

D O I：

10.1006/bbrc.2001.5312

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In this study we analyzed the role of vascular NAD(P)H oxidase in the generation of O-2(-) and the endothelial impairment of NO signal transduction pathway in hypertension. In aortic rings of 15-month-old stroke-prone spontaneously hypertensive rats (SHR15) we found a 10-fold increased expression of NAD(P)H oxidase subunit gp91phox mRNA associated with a 3-fold increased production of O-2(-) compared to age-matched Wistar rats (WIS15). Vasorelaxation studies in aortas of SHR15 showed a strongly diminished response to acetylcholine, NO-donor S-nitroso-N-acetyl-D,L-penicillamine, and organic nitrate glyceryl trinitrate compared to WIS15. Soluble guanylate cyclase (sGC activity and sGC beta (1)-subunit protein expression was downregulated in aortas and lungs of SHR15. These data suggest an upregulation of vascular NAD(P)H oxidase and an impairment of the NO signal transduction pathway in hypertension. (C) 2001 Academic Press.

引用

页码：1130 / 1135

页数：6

共 53 条

[1]

AHLNER J, 1991, PHARMACOL REV, V43, P351

[2]

ALLEN RC, 1986, METHOD ENZYMOL, V133, P449

[3] Vasodilator dysfunction in aged spontaneously hypertensive rats:: changes in NO synthase III and soluble guanylyl cyclase expression, and in superoxide anion production [J].