Gene Expression of Endothelial Type Isoform of Nitric Oxide Synthase in Various Tissues of Stroke-Prone Spontaneously Hypertensive Rats

Toshirou Seki; Mitsuhide Naruse; Kiyoko Naruse; Takeshi Katafuchi; Khalid Mahmud Lodhi; Takanobu Yoshimoto; Hiromi Hagiwara; Hiroshi Demura; Shigehisa Hirose

doi:10.1291/hypres.20.43

Toshirou Seki, Mitsuhide Naruse, Kiyoko Naruse, Takeshi Katafuchi, Khalid Mahmud Lodhi, Takanobu Yoshimoto, Hiromi Hagiwara, Hiroshi Demura, Shigehisa Hirose

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Toshirou Seki
the Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
Mitsuhide Naruse
the Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
Kiyoko Naruse
the Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
Takeshi Katafuchi
Department of Biological Sciences, Tokyo Institute of Technology
Khalid Mahmud Lodhi
Department of Biological Sciences, Tokyo Institute of Technology
Takanobu Yoshimoto
the Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
Hiromi Hagiwara
Research Center for Experimental Biology,Tokyo Institute of Technology
Hiroshi Demura
the Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical College
Shigehisa Hirose
Department of Biological Sciences, Tokyo Institute of Technology

Keywords: nitric oxide, nitric oxide synthase, gene expression, stroke-prone spontaneously hypertensive

JOURNAL FREE ACCESS

1997 Volume 20 Issue 1 Pages 43-49

DOI https://doi.org/10.1291/hypres.20.43

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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 5wk or 13wk 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. (Hypertens Res 1997; 20: 43-49)

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