Deoxycorticosterone Acetate Plus Salt Induces Overexpression of Vascular Endothelin-1 and Severe Vascular Hypertrophy in Spontaneously Hypertensive Rats
Autor: | Pavol Sventek, Jin S. Li, Ernesto L. Schiffrin, Rhian M. Touyz, Richard Larivière |
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Rok vydání: | 1995 |
Předmět: |
Male
medicine.hormone medicine.medical_specialty Systole Blood Pressure Sodium Chloride Muscle hypertrophy Rats Sprague-Dawley Endothelins Rats Inbred SHR medicine.artery Internal medicine Internal Medicine medicine Animals RNA Messenger cardiovascular diseases Desoxycorticosterone Mesenteric arteries Aorta business.industry Vascular disease Body Weight Arteries Hypertrophy medicine.disease Endothelin 1 Mesenteric Arteries Rats medicine.anatomical_structure Endocrinology cardiovascular system Vascular resistance business circulatory and respiratory physiology Artery |
Zdroj: | Hypertension. 25:769-773 |
ISSN: | 1524-4563 0194-911X |
DOI: | 10.1161/01.hyp.25.4.769 |
Popis: | Abstract Endothelin-1 gene expression is enhanced in the aorta and mesenteric arteries, and possibly other vessels, of deoxycorticosterone acetate (DOCA)–salt hypertensive rats. In contrast, endothelin-1 gene expression is normal or reduced in spontaneously hypertensive rats (SHR). Severe vascular hypertrophy is present in DOCA-salt hypertensive rats but not in SHR. In this study we investigated whether treatment of SHR with DOCA and salt would result in enhanced endothelin-1 expression and at the same time in severe vascular hypertrophy. Increased abundance of endothelin-1 mRNA was found in the aorta and the mesenteric arterial bed of SHR treated simultaneously with DOCA and salt but not when rats were treated with either separately. The wet weight of the aorta and of the mesenteric arterial bed, media thickness, media cross-sectional area, and media-to-lumen ratio of mesenteric small arteries of DOCA- salt–treated SHR were exaggerated beyond what could be explained by the elevation of blood pressure, relative to SHR treated with salt or with DOCA, which did not overexpress vascular endothelin-1. In conclusion, SHR may exhibit enhanced expression of the endothelin-1 gene in blood vessels when treated with DOCA and salt, and associated with this there is severe vascular hypertrophy. These data support the hypothesis of a role of endothelin-1 in vascular hypertrophy. |
Databáze: | OpenAIRE |
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