Journal
EUROPACE
Volume 14, Issue 8, Pages 1206-1214Publisher
OXFORD UNIV PRESS
DOI: 10.1093/europace/eus052
Keywords
Angiotensin receptor blocker; Atrial fibrillation; Connective tissue growth factor; Rapid pacing
Categories
Funding
- Grants-in-Aid for Scientific Research [23591061] Funding Source: KAKEN
Ask authors/readers for more resources
Remodelling of the extracellular matrix (ECM) plays an important role in the production of arrhythmogenic substrate for atrial fibrillation (AF), and is considered to be promoted by the connective tissue growth factor (CTGF). Our objective was to assess the relationship between CTGF and ECM synthesis, and the effect of olmesartan on these processes. Fifteen canine AF models were produced by rapid atrial stimulation. They were divided into three groups: pacing control (n 5): 6-week pacing, pacing olmesartan (n 5): pacing with olmesartan (2 mg/kg/day), and non-pacing group (n 5). In the pacing control group, messenger ribonucleic acid expressions of CTGF and collagen types 1 and 3 were up-regulated in comparison with the non-pacing group (P 0.05) while transforming growth factor- (TGF-) did not exhibit a significant difference. In the pacing olmesartan group, these up-regulations were suppressed (P 0.05). In fluorescent immunostaining, the expression of CTGF was localized in the cytoplasm. The protein level of collagen type 3 was increased in the pacing control and it was suppressed in the pacing olmesartan group. CTGF and associated genes were up-regulated in the atria with the appearance of fibrosis. Because this up-regulation was independent of TGF- and suppressed by olmesartan, CTGF up-regulation was considered to be mediated by angiotensin II.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available