Effect of Angiotensin-(1-7) on Aortic Response, TNF-α, IL-1β and Receptor for Advanced Glycation Endproduct in Rat's Adjuvant-Induced Arthritis

Açikalin, Öznur; Bölükbaşi Hatip, Funda F.; Tan, Ruyal F.; Hatip-al-Khatib, Izzettin
March 2016
Pharmacology;3/15/2016, Vol. 97 Issue 5/6, p207
Academic Journal
Altered vascular reactivity due to endothelial dysfunction, consequent to vascular damage, is observed in rheumatoid arthritis. We investigated the effect of angiotensin (Ang)-(1- 7) on vasculature changes in arthritis induced by complete Freund's adjuvant in male Wistar rats. Arthritis decreased soluble receptor for advanced glycation end products (sRAGE) whereas elevated aortic RAGE expression, increased interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), systolic blood pressure and the contractility induced by phenylephrine and KCl. Moreover, arthritis decreased the relaxing effect of acetylcholine. Neither arthritis nor Ang-(1-7) altered sodium nitroprusside relaxation. Ang-(1-7) reversed the effect of arthritis on TNF-α, sRAGE and RAGE expression without any effect on the IL-1β. Ang-(1-7) decreased phenylephrine and KCl contractility, especially in the endothelial- denuded aorta, whereas increased acetylcholine relaxation in the endothelial-intact aorta. Ang-(1-7) could find its place in the treatment protocol of arthritis and vascular diseases.


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