Control of oxidative stress in microcirculation of spontaneously hypertensive rats

Microcirculation Laboratory, Department of Bioengineering and The Whitaker Institute of Biomedical Engineering, University of California San Diego, La Jolla, California Submitted 14 July 2004 ; accepted in final form 28 September 2004 One mechanism for organ damage in individuals with arterial hyper...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2005-02, Vol.288 (2), p.H805-H812
Hauptverfasser: DeLano, F. A, Balete, R, Schmid-Schonbein, G. W
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Sprache:eng
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Zusammenfassung:Microcirculation Laboratory, Department of Bioengineering and The Whitaker Institute of Biomedical Engineering, University of California San Diego, La Jolla, California Submitted 14 July 2004 ; accepted in final form 28 September 2004 One mechanism for organ damage in individuals with arterial hypertension may be due to oxygen free radical production. This study was designed to localize free radicals in a microvascular network of mature spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats. Because glucocorticoids play a role in pressure elevation of SHRs, we investigated their role in microvascular free radical formation. Oxygen radical production in mesentery was detected by tetranitroblue tetrazolium reduction to formazan aided by digital light-absorption measurements. Formazan deposits were observed in the endothelial cells and lumens of all microvessels and in lymphatic endothelia but were fewer in tissue parenchyma. The formazan distribution in younger (14–16 wk old) WKY rats and SHRs was heterogeneous with low values in capillaries and small arterioles/venules (
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.00696.2004