Effect of Angiotensin-(1-7) on Aortic Response, TNF-α, IL-1β and Receptor for Advanced Glycation Endproduct in Rat's Adjuvant-Induced Arthritis
| Autor: | Açikalin Ö, Bölükbaşi Hatip FF, Tan RF, Hatip-Al-Khatib I |
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| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
cardiovascular system
Acetylcholine/pharmacology Angiotensin I/pharmacology/therapeutic use Animals Aorta Thoracic/*drug effects/metabolism/physiology Arthritis Experimental/blood/drug therapy/metabolism/physiopathology Blood Pressure/drug effects Interleukin-1beta/*blood Male Peptide Fragments/pharmacology/therapeutic use Phenylephrine/pharmacology Potassium Chloride/pharmacology Rats Sprague-Dawley Rats Wistar Receptor for Advanced Glycation End Products/blood/*metabolism Tumor Necrosis Factor |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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