Effect of Vitamin E on Vascular Responses of Thoracic Aorta in Rat Experimental Arthritis

Cinar, MG; Can, Cenk; Ülker, Sibel; Gök, Şule; Çöker, Canan; Soykan, Necdet; Koşay, Sezen; Evinç, Akgün

doi:10.1016/s0306-3623(97)00387-x

Cited by 12 publications

(12 citation statements)

References 10 publications

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“…In the present study, we investigated endothelial function in the AIA model, which is commonly accepted as having many histologic and clinical features in common with human RA (31) and which is widely used to predict clinical efficacy of new therapies in RA (32). In accordance with previous studies (12)(13)(14)(15)(16)(33)(34)(35), our data show that endothelial function assessed by the vasodilating response to ACh is impaired in AIA rats. We also demonstrated that endothelial dysfunction correlates with disease activity.…”

Section: Discussionsupporting

confidence: 80%

“…In the model of adjuvant-induced arthritis (AIA), data demonstrated that vessels from AIA rats overproduced superoxide anions (O 2 Ϫ ) (12)(13)(14) and that BH 4 supplementation decreased endothelial dysfunction (12), suggesting that the deficiency in BH 4 may contribute to the uncoupling of eNOS and subsequent production of O 2 Ϫ . However, treatment with vitamin E used as an antioxidant both improved (15) and decreased (16) endothelial function in AIA rats. To our knowledge, it is currently not known whether a deficit in NO availability accounts for arthritis-associated endothelial dysfunction.…”

mentioning

confidence: 92%

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Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Prati¹,

Berthelot²,

Wendling³

et al. 2011

Arthritis & Rheumatism

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Objective. To investigate whether arginase pathway abnormalities occur in vessels from rats with adjuvant-induced arthritis (AIA), and to determine whether the up-regulation of arginase, which reciprocally regulates nitric oxide synthase (NOS) by competing for the same substrate, L-arginine, contributes to endothelial dysfunction in AIA.Methods. We performed vascular reactivity experiments on thoracic aortic rings from AIA rats and control rats, and we investigated the response of rings to norepinephrine (NE), sodium nitroprusside (SNP), and acetylcholine (ACh). ACh-induced relaxation was evaluated in the presence (or not in the presence) of the NOS inhibitor N G -nitro-L-arginine methyl ester (L-NAME), the arginase inhibitor N -hydroxy-nor-Larginine (nor-NOHA), or both. Aortic arginase activity was measured using a spectrophotometric method, and the expression of arginase and endothelial NOS (eNOS) was evaluated by Western blotting.Results. ACh-induced vasodilation was significantly impaired in AIA rats, while the responses to NE and to SNP did not differ from those in control rats. L-NAME reduced ACh-induced vasodilation to a lesser extent in AIA rats than in control rats. Incubation of aortic rings with nor-NOHA enhanced the vascular response to ACh in AIA rats and reversed the effects of L-NAME. Compared with control rats, AIA rats exhibited increased vascular expression of arginase II (by 22%) (P < 0.05) as well as increased arginase activity (by 49%) (P < 0.05), whereas eNOS expression was unchanged. Finally, arginase activity and expression correlated positively with arthritis severity.Conclusion. Our results are consistent with the notion that arginase up-regulation plays a role in AIAassociated endothelial dysfunction. They suggest that arginase might be an attractive new target for treating endothelial dysfunction in arthritis.

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Section: Discussionsupporting

confidence: 80%

mentioning

confidence: 92%

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Prati¹,

Berthelot²,

Wendling³

et al. 2011

Arthritis & Rheumatism

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“…Similarly, a recent study by Palmer et al [33] has reported a deleterious effect of vitamin E supplementation on vascular impairment in mesenteric arteries of STZ-diabetic rats. It has previously been shown by our laboratory that vitamin E administration to experimental arthritic rats failed to restore adjuvant-induced abnormalities in vascular function, while it provided ameliorating effects in improving systemic signs of arthritis [21]. A deleterious effect of higher doses of vitamin E on the defective endothelium-dependent relaxation has also been reported in hypercholesterolemic rabbits [34].…”

Section: Discussionmentioning

confidence: 93%

“…STZ was injected to the rats in the resting two groups, one of which was fed standard diet; the second was fed a diet containing 1,000 mg/kg chow vitamin E. The duration of treatment period was 12 weeks, since macrovascular alterations of diabetes were reported to be settled during this time period [20]. It has been previously reported by our laboratory that vitamin E administration to control rats did not change the vascular responses significantly [21]. A pilot study on normal age-matched rats was carried out to determine the effect of dietary vitamin E supplementation; since no change in vascular responses was observed in this preliminary study, data are not shown.…”

Section: Induction Of Diabetes and Study Groupsmentioning

confidence: 99%

Effect of Dietary Vitamin E Supplementationon Vascular Reactivity of Thoracic Aorta in Streptozotocin-Diabetic Rats

Çınar¹,

Ülker²,

Alper

et al. 2001

Pharmacology

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The present study evaluated the effect of dietary vitamin E supplementation (1,000 mg/kg chow) on the alterations in vascular reactivity of streptozotocin-diabetic aorta of Wistar rats. After 12 weeks of treatment, thoracic aortic rings of rats were mounted in organ baths and contractile responses to phenylephrine and 5-hydroxytryptamine and relaxant responses to acetylcholine, calcium ionophore and sodium nitroprusside were assessed. Plasma vitamin E concentration as measured by HPLC was markedly decreased in diabetic rats and increased with dietary vitamin E supplementation. Induction of diabetes significantly impaired endothelium-dependent relaxations to acetylcholine and calcium ionophore in aortic rings, but did not change endothelium-independent relaxation to sodium nitroprusside. Vitamin E significantly improved the impaired endothelium-dependent relaxations, further it decreased the enhanced contractile response to phenylephrine and 5-hydroxytryptamine in diabetic rings. The mechanical denudation of endothelium or the chemical inhibition of endothelium-dependent relaxation with N^ω-nitro-L-arginine methyl ester (100 µmol/l) significantly increased phenylephrine contractility in control rings and the rings of diabetic rats treated with vitamin E; such a difference was not observed in diabetic rats fed with normal diet. Liver and lung malondialdehyde concentrations, as an index of lipid peroxidation, were increased in diabetic rats and significantly decreased with vitamin E supplementation. It is concluded that dietary supplementation of vitamin E improved endothelial dysfunction in insulin-dependent model of uncontrolled diabetes, probably decreasing membranal lipid peroxidation.

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“…Inflammatory reactions are characterized by polymorphonuclear leukocyte infiltration as well as vascular damage with increased vascular permeability [1,2]. An enhanced reactivity of vascular smooth muscle to several contractile agonists with a diminished endothelium-derived relaxation has also been demonstrated in adjuvant arthritis models [3][4][5] and this was attributed to the production of oxygen free radicals or cytokines by inflammatory cells in response to mycobacteria infections [1,4]. It has recently been reported that experimental avidin-induced polyarthritis is associated with a pronounced coronary vasoconstriction in rat hearts perfused in vitro [6].…”

Section: Introductionmentioning

confidence: 99%

Role of Leukotrienes on Coronary Vasoconstriction in Isolated Hearts of Arthritic Rats: Effect of in vivo Treatment with CI-986, a Dual Inhibitor of Cyclooxygenase and Lipoxygenase

Gök

Ülker²,

Hüseyinov

et al. 2000

Pharmacology

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In this study, coronary perfusion pressure and force of contraction were investigated in isolated hearts removed from arthritic rats by using the Langendorff method. A strong coronary vasoconstriction was determined in arthritic hearts which was associated with elevated levels of arachidonate 5-lipoxygenase (5-LOX) products, leukotriene B₄ (LTB₄) and LTC₄ in coronary effluents. In vivo treatment with the dual inhibitor of cyclooxygenase (COX) and LOX, CI-986 (2 and 10 mg/kg/day) on days 14– 26 following adjuvant injection, prevented the coronary vasoconstriction and the increased production of LTB₄ and LTC₄. These results suggest that the coronary vasoconstriction in the isolated arthritic hearts is associated with an increased activity of the LOX system and CI-986 could have a preventive effect on constriction of coronary arteries.

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Effect of Vitamin E on Vascular Responses of Thoracic Aorta in Rat Experimental Arthritis

Cited by 12 publications

References 10 publications

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Endothelial dysfunction in rat adjuvant‐induced arthritis: Up‐regulation of the vascular arginase pathway

Effect of Dietary Vitamin E Supplementationon Vascular Reactivity of Thoracic Aorta in Streptozotocin-Diabetic Rats

Role of Leukotrienes on Coronary Vasoconstriction in Isolated Hearts of Arthritic Rats: Effect of in vivo Treatment with CI-986, a Dual Inhibitor of Cyclooxygenase and Lipoxygenase

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