Open AccessEffects of the Galanin Receptor Antagonist M40 on Cardiac Function and Remodeling in Rats with Heart Failure
Author(s) -
Chen Ao,
Li Min,
Song Lei,
Zhang Yunhe,
Luo Zhangyuan,
Zhang Wenzan,
Chen Yingmin,
He Ben
Publication year - 2015
Publication title -
cardiovascular therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 46
eISSN - 1755-5922
pISSN - 1755-5914
DOI - 10.1111/1755-5922.12144
Subject(s) - medicine , galanin , heart failure , endocrinology , cardioprotection , cardiac function curve , brain natriuretic peptide , myocardial infarction , receptor , neuropeptide
Summary Background Sympathetic activation and parasympathetic withdrawal are important characteristics of heart failure. Recent studies demonstrate that galanin reduces the discharge of acetylcholine and inhibits vagal bradycardia by acting on galanin receptor type 1 (GalR1). We speculated that blocking GalR1 is beneficial for heart failure. Methods Rats with heart failure were induced by myocardial infarction. The rats were injected intraperitoneally with galanin receptor antagonist M40 solution (30 nmol/kg) or saline for 4 weeks. Cardiac function was assessed by echocardiography and brain natriuretic peptide ( BNP ) in plasma. The ratio of heart weight to body weight ( HW / BW ), hematoxylin–eosin ( HE ), and Masson trichrome stain was used to evaluate cardiac remodeling. Tumor necrosis factor‐ α ( TNF ‐ α ), interleukin 6 ( IL ‐6) in plasma, and sarco(endo)plasmic reticulum Ca 2+ ‐ ATP ase ( SERCA 2) in heart tissue were detected to confirm the mechanism of the cardioprotection effect. Results Compared with rats injected with saline, M40 effectively improved cardiac function of contraction; decreased BNP , IL ‐6, and HW / BW (all P < 0.05); attenuated cardiac fibrosis; and upregulated SERCA 2 ( P < 0.05). Conclusion M40 improves cardiac function and attenuates remodeling, suggesting that galanin receptor antagonist may be a potential therapeutic agent for HF .