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易卒中型自发性高血压大鼠不同组织中一氧化氮合酶内皮型同工型的基因表达

Gene expression of endothelial type isoform of nitric oxide synthase in various tissues of stroke-prone spontaneously hypertensive rats.

作者信息

Seki T, Naruse M, Naruse K, Katafuchi T, Lodhi K M, Yoshimoto T, Hagiwara H, Demura H, Hirose S

机构信息

Department of Medicine, Tokyo Women's Medical College, Japan.

出版信息

Hypertens Res. 1997 Mar;20(1):43-9. doi: 10.1291/hypres.20.43.

DOI:10.1291/hypres.20.43
PMID:9101312
Abstract

Nitric oxide (NO) has been suggested to play important roles in the pathophysiology of various cardiovascular diseases. This study tested the hypothesis that an attenuated biological action of NO in hypertension is attributed to a change in the gene expression of NO synthase (NOS), a key enzyme involved in NO formation. The expression level of mRNA of endothelial type NOS (NOS-III) was determined in stroke-prone spontaneously hypertensive rats (SHR-SP/Izm) and Wistar Kyoto rats (WKY/Izm) by ribonuclease protection assay using a partial clone as probe. NOS-III mRNA was expressed ubiquitously in various tissues of WKY/Izm and SHR-SP/Izm either at 5 wk or 13 wk of age. There was no significant difference in the tissue expression of NOS-III mRNA between the two strains at either age. The intensity and localization of the hybridization signal for NOS-III mRNA in the heart of SHR-SP/Izm did not differ from those in the heart of WKY/Izm. These results suggest that the attenuated biological action of NO implied in genetically hypertensive rats is not attributed to an abnormality at the level of NOS-III mRNA expression in the tissues, although lack of an increase in NOS-III gene expression, despite the hypertensive hemodynamic stress, may modify the blood pressure in hypertension.

摘要

一氧化氮(NO)被认为在各种心血管疾病的病理生理学中发挥重要作用。本研究检验了以下假设:高血压中NO生物作用减弱归因于参与NO生成的关键酶——一氧化氮合酶(NOS)基因表达的改变。使用部分克隆作为探针,通过核糖核酸酶保护试验,测定了易中风自发性高血压大鼠(SHR-SP/Izm)和Wistar Kyoto大鼠(WKY/Izm)中内皮型NOS(NOS-III)的mRNA表达水平。在5周龄或13周龄时,NOS-III mRNA在WKY/Izm和SHR-SP/Izm的各种组织中均有普遍表达。在这两个年龄段,两品系之间NOS-III mRNA的组织表达均无显著差异。SHR-SP/Izm心脏中NOS-III mRNA的杂交信号强度和定位与WKY/Izm心脏中的无差异。这些结果表明,遗传性高血压大鼠中所暗示的NO生物作用减弱并非归因于组织中NOS-III mRNA表达水平的异常,尽管在高血压血流动力学应激下NOS-III基因表达缺乏增加可能会改变高血压中的血压。

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