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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, OBJECTIVE, RESULTS. Meshes: Angiotensin II Type 1 Receptor Blockers, Animals, Arrhythmias, Cardiac, Benzimidazoles, Connective Tissue Growth Factor, Diabetes Mellitus, Experimental, Female, Fibrosis, Heart Atria, Rats, Rats, Sprague-Dawley, Receptor for Advanced Glycation End Products, Tetrazoles.
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Does angiotensin II type 1 receptor blocker attenuate diabetes-induced atrial structural remodeling? Context: Diabetes mellitus promotes atrial structural remodeling, thereby producing atrial arrhythmogenicity, where advanced glycation endproducts (AGEs) and their receptor (RAGE) are implicated to play a role in the pathogenesis. We investigated the effects of candesartan, an angiotensin type II receptor blocker, on the diabetes-induced atrial structural change. Diabetes was induced in 8-week-old female Sprague-Dawley rats by intraperitoneal injection of streptozotocin at 70 mg/kg. Osmotic pumps were simultaneously set to infuse candesartan at a subdepressor dose of 0.05 mg/kg/day. Twelve weeks after the induction of diabetes, the blood glucose and glycated hemoglobin A1c were significantly higher in streptozotocin-injected rats than those in control rats, and were not affected by candesartan treatment. The atria of diabetic rats showed remarkable diffuse interstitial fibrosis with more enhanced protein expressions of RAGE and connective tissue growth factor (CTGF) compared with control ones. The treatment with candesartan significantly reduced CTGF expression and effectively suppressed the development of fibrotic deposition in diabetic animals.
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Candesartan reduced CTGF expression and attenuated the fibrosis in diabetic rat atria. These results implied the protective effects of candesartan on diabetes-related atrial arrhythmias. Final Decision: yes