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Ultrastructural characteristics of aortic endothelial cells in borderline hypertensive rats exposed to chronic social stress
L. Okruhlicová, K. Dlugosová, M. Mitasíková, I. Bernátová
Language English Country Czech Republic
Document type Journal Article, Research Support, Non-U.S. Gov't
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- MeSH
- Aorta, Thoracic enzymology ultrastructure MeSH
- Behavior, Animal * MeSH
- Chronic Disease MeSH
- Endothelial Cells enzymology ultrastructure MeSH
- Hypertension genetics metabolism pathology physiopathology psychology MeSH
- Blood Pressure MeSH
- Rats MeSH
- Disease Models, Animal MeSH
- Crowding * MeSH
- Rats, Inbred SHR MeSH
- Rats, Wistar MeSH
- Disease Progression MeSH
- Stress, Psychological metabolism pathology physiopathology MeSH
- Nitric Oxide Synthase metabolism MeSH
- Microscopy, Electron, Transmission MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Genetic predisposition and social stress may represent important risk factors in etiology of hypertension associated with endothelial dysfunction. Perturbations of endothelial structural integrity are also critical for the pathogenesis of vascular diseases. We examined effect of chronic social stress on structure of aortic endothelium in borderline hypertensive (BHR) and normotensive Wistar rats. Male BHR - offspring of Wistar mothers and SHR fathers and age-matched W were exposed to 6-week crowding stress (5 rats/cage, 200 cm2/rat). Aortic tissue was processed for electron microscopy and NO synthase activity measurement. Crowding stress significantly increased blood pressure in BHR compared to basal values (140+/-3 mm Hg vs. 130+/-3 mm Hg, p<0.05) and reduced enzyme activity by 37 % (p<0.01) in the aorta of BHR. Local slight structural alterations of endothelium were found in non-stressed BHR (p<0.001) when compared with Wistar rats. Chronic stress caused marked (p<0.005) subcellular injury of endothelial cells in aorta of BHR characterized by mitochondrial damage, presence of vacuoles, increased number of lysosomes, Weibel-Palade bodies, changes of intercellular connections and local disruption of endothelium, while only slight changes were seen in Wistar rats. Results suggest increased sensitivity of aortic endothelium of BHR to chronic crowding that may contribute to acceleration of arterial dysfunction.
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