期刊
JOURNAL OF INTERFERON AND CYTOKINE RESEARCH
卷 34, 期 11, 页码 870-875出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/jir.2013.0159
关键词
-
The central mechanisms by which interleukin-1 beta (IL-1 beta) and angiotension II receptor 1 (AT1-R) contribute to sympathoexcitation in heart failure (HF) are unclear. In this study, we determined whether an interaction between IL-1 beta and AT1-R in the paraventricular nucleus (PVN) contributes to progression of HF. Rats were implanted with bilateral PVN cannulae and subjected to coronary artery ligation or sham surgery (Sham). Subsequently, animals were treated for 4 weeks through PVN infusion with either vehicle, losartan (LOS, 200 mu g/day), IL-1 beta (IL, 1 mu g/day), or IL-1 beta along with LOS (LOS+IL). HF rats had higher levels of corticotropin-releasing hormone (CRH), norepinephrine (NE), and glutamate (Glu); lower levels of gamma-aminobutyric acid (GABA); and more positive fra-like activity in PVN when compared with Sham rats. HF rats also had higher levels of NE, epinephrine (EPI), and IL-1 beta in plasma. PVN infusion of LOS attenuated the decreases in GABA and the increases in CRH, NE, and Glu in the PVN of HF rats. IL-1 beta could further increase the expression of CRH, NE, Glu, EPI, and IL-1 beta and decrease GABA expression. Treatment with IL-1 beta along with LOS could eliminate the effects of IL-1 beta. These findings suggest that an interaction between AT1-R and IL-1 beta in the PVN contributes to progression in HF.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据