Antioxidant-rich diet relieves hypertension and reduces renal immune infiltration in spontaneously hypertensive rats
- PMID: 12574105
- DOI: 10.1161/01.hyp.0000052833.20759.64
Antioxidant-rich diet relieves hypertension and reduces renal immune infiltration in spontaneously hypertensive rats
Abstract
Previous studies have demonstrated that oxidative stress contributes to hypertension and treatments with either antioxidant or immunosuppressive/anti-inflammatory agents improve hypertension in spontaneously hypertensive rats (SHR). The present study was performed to determine if the antihypertensive effects of an antioxidant-rich diet are associated with reduction in the renal immune infiltration. Rats were divided into experimental groups (n=5 each) that were followed 7 months after birth, during which they were fed either a regular or antioxidant-enriched (test) diet as follows: SHR-R group=regular diet; SHR-T group=test diet throughout the experiment; SHR-S group=test diet for 4 months switched to regular diet thereafter; WKY group=control rats given regular diet. The SHR-T rats showed a significant reduction in systolic blood pressure (mm Hg): SHR-T=179.6+/-12.9 versus SHR-R=207.5+/-9.6 (P<0.001) and plasma hydrogen peroxide concentration (SHR-T=15+/-4 micro mol/L versus 34+/-9 in SHR-R rats). This was accompanied by significant reductions of renal tissue nitrotyrosine abundance, tubulointerstitial infiltration (cells/mm(2)) of lymphocytes (SHR-T=18+/-3 versus SHR-R=30+/-4, P<0.001), macrophages (SHR-T= 17+/-3 versus SHR-R=22+/-3), and angiotensin II-positive cells (SHR-T= 17+/-2 versus SHR-R=25+/-5, P<0.01). Results in the SHR-S group were intermediate between the SHR-R and SHR-T groups. The intensity of the infiltration of lymphocytes, macrophages, and angiotensin II-positive cells significantly correlated with systolic blood pressure. Thus, the present study demonstrates that an antioxidant-enriched diet reduces the renal interstitial inflammation and improves hypertension in SHR. These findings point to interrelation between oxidative stress and inflammatory reactivity in the pathogenesis of hypertension.
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