Vascular Structure and Expression of Endothelin-1 Gene in L-NAME–Treated Spontaneously Hypertensive Rats
Autor: | Christian F. Deschepper, Kevin L. Grove, Pavol Sventek, Ernesto L. Schiffrin, Jin S. Li |
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Rok vydání: | 1996 |
Předmět: |
medicine.medical_specialty
Systole Molecular Sequence Data Gene Expression Blood Pressure Arginine Muscle hypertrophy Nitric oxide chemistry.chemical_compound Rats Inbred SHR medicine.artery Internal medicine Internal Medicine medicine Animals Enzyme Inhibitors Aorta Base Sequence biology business.industry Endothelins Body Weight Endothelium-derived relaxing factor Heart Hypertrophy Organ Size Endothelin 1 Rats Nitric oxide synthase NG-Nitroarginine Methyl Ester medicine.anatomical_structure Endocrinology Blood pressure chemistry cardiovascular system biology.protein Blood Vessels Nitric Oxide Synthase business Blood vessel |
Zdroj: | Hypertension. 27:49-55 |
ISSN: | 1524-4563 0194-911X |
DOI: | 10.1161/01.hyp.27.1.49 |
Popis: | Abstract Inhibition of nitric oxide synthase by l -arginine analogues is associated with elevation of blood pressure in rats. Deoxycorticosterone acetate (DOCA)-salt hypertensive rats and DOCA-salt–treated spontaneously hypertensive rats (SHR) overexpress the endothelin-1 gene in blood vessels, and this is associated with severe vascular hypertrophy, whereas SHR do not overexpress endothelin-1 and exhibit limited vascular hypertrophy. In this study malignant hypertension was induced in SHR by chronic administration of the l -arginine analogue N G -nitro- l -arginine methyl ester (L-NAME), a potent inhibitor of nitric oxide synthase, to determine whether malignant hypertension would result in endothelin-1 gene overexpression in blood vessels and in greater severity of vascular hypertrophy, as found in malignant DOCA-salt–treated SHR. L-NAME treatment induced malignant hypertension in SHR, with a systolic blood pressure of 246±2 mm Hg, compared with 211±2 mm Hg ( P P |
Databáze: | OpenAIRE |
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