title: Gene expression of endothelial type isoform of nitric oxide synthase in various tissues of stroke-prone spontaneously hypertensive rats.
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.
authors.affiliation: Department of Medicine, Tokyo Women's Medical College, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Seki
authors.forename: M
authors.initials: M
authors.lastname: Naruse
authors.forename: K
authors.initials: K
authors.lastname: Naruse
authors.forename: T
authors.initials: T
authors.lastname: Katafuchi
authors.forename: K M
authors.initials: KM
authors.lastname: Lodhi
authors.forename: T
authors.initials: T
authors.lastname: Yoshimoto
authors.forename: H
authors.initials: H
authors.lastname: Hagiwara
authors.forename: H
authors.initials: H
authors.lastname: Demura
authors.forename: S
authors.initials: S
authors.lastname: Hirose
mesh_terms: D000818:Animals; D002561:Cerebrovascular Disorders / Q000201:enzymology / Q000235:genetics*; D004730:Endothelium, Vascular / Q000201:enzymology*; D015971:Gene Expression Regulation, Enzymologic / Q000502:physiology*; D006973:Hypertension / Q000201:enzymology / Q000235:genetics*; D017403:In Situ Hybridization; D007527:Isoenzymes / Q000096:biosynthesis* / Q000235:genetics*; D009206:Myocardium / Q000201:enzymology; D019001:Nitric Oxide Synthase / Q000096:biosynthesis* / Q000235:genetics*; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012260:Ribonucleases / Q000037:antagonists & inhibitors
chemical_list: D007527:Isoenzymes; D012333:RNA, Messenger; D019001:Nitric Oxide Synthase; D012260:Ribonucleases