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Abstract
Chronic beta-adrenergic blockade prevents volume overload-induced re-localization and oxidation of soluble guanylyl cyclase
Highlights
While b-adrenergic blockade is a cornerstone of heart failure therapy, its therapeutic role in chronic mitral regurgitation remains questionable
Expression, localization, cyclase activity, and redox state of myocardial soluble guanylyl cyclase (sGC) were assessed in Control, mitral regurgitation (MR), and MR+bB dogs
* Correspondence: emily.tsai@tuhs.temple.edu 1Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA, 19140, USA Full list of author information is available at the end of the article total sGCa1 expression fell to nearly 50% of Control and re-localized away from Cav3+LR to non-lipid raft microdomains (NLR)
Summary
While b-adrenergic blockade is a cornerstone of heart failure therapy, its therapeutic role in chronic mitral regurgitation remains questionable. Materials and methods Volume-overload (VO) was established by chordal ruptureinduced mitral regurgitation (MR) in mongrel dogs. Some dogs were treated with metoprolol succinate (100mg orally once daily; MR+ bB).
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