Candesartan ameliorates arsenic-induced hypertensive vascular remodeling by regularizing angiotensin II and TGF-beta signaling in rats

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• 作者：Maibam Wanta Khuman^a ; Sankaran Kutty Harikumar^a ; Abdul Sadam^a ; Manickam Kesavan^a ; Vattaparambil Sukumaran Susanth^a ; Subhashree Parida^a ; Karam Pal Singh^b ; Souvendra Nath Sarkar^a ; ^{snsarkar1911@gmail.com}
• 关键词：AngII ; angiotensin II ; ARB ; angiotensin receptor blocker ; AT1R ; AT1 receptor ; AT2R ; AT2 receptor ; CVD ; cardiovascular disease ; DBP ; diastolic blood pressure ; CMC ; carboxymethyl cellulose ; CTGF ; connective tissue growth factor ; ECM ; extracellular matrix ; eNOS ; endothelial nitric oxide synthase ; ERK ; extracellular signal-regulated kinase ; FGF ; fibroblast growth factor ; IHC ; immunohistochemistry ; MAP ; mean arterial pressure ; MAPK ; mitogen-activated protein kinase ; PBS ; phosphate-buffered saline ; PD
• 刊名：Toxicology
• 出版年：2016
• 出版时间：30 December 2016
• 年：2016
• 卷：374
• 期：Complete
• 页码：29-41
• 全文大小：4057 K
• 卷排序：374

文摘

Examined whether candesartan can ameliorate arsenic-induced vascular disorders. Arsenic caused systemic hypertension & also enhanced AngII-induced blood pressure. Arsenic elevated AngII & TGF-β levels; up-regulated aortic AT1 & TβRII receptors. Also increased transducers of MAPK & TGF-β pathways, aortic collagen & thickness. Candesartan reduced arsenic-induced functional, biochemical & structural changes.