ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2014
Interaction between interleukin-1 beta and angiotensin II receptor 1 in hypothalamic paraventricular nucleus contributes to progression of heart failure.
Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
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- NETs Lead to Sympathetic Hyperactivity After Traumatic Brain Injury Through the LL37-Hippo/MST1 Pathway.Frontiers in neuroscience · 2021Article
- Immunomodulatory Approaches in Diabetes-Induced Cardiorenal Syndromes.Frontiers in cardiovascular medicine · 2020Review
- Role of interleukins in heart failure with reduced ejection fraction.Anatolian journal of cardiology · 2019Review
- Preventive and Therapeutic Role of Functional Ingredients of Barley Grass for Chronic Diseases in Human Beings.Oxidative medicine and cellular longevity · 2018Review
- Age-dependent alterations to paraventricular nucleus insulin-like growth factor 1 receptor as a possible link between sympathoexcitation and inflammation.Journal of neurochemistry · 2016Article
- Sympathoexcitation in Rats With Chronic Heart Failure Depends on Homeobox D10 and MicroRNA-7b Inhibiting GABBR1 Translation in Paraventricular Nucleus.Circulation. Heart failure · 2016Article
- Brain endogenous angiotensin II receptor type 2 (AT2-R) protects against DOCA/salt-induced hypertension in female rats.Journal of neuroinflammation · 2015Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The central mechanisms by which interleukin-1 beta (IL-1β) 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-1β 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 μg/day), IL-1β (IL, 1 μg/day), or IL-1β 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-1β 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-1β could further increase the expression of CRH, NE, Glu, EPI, and IL-1β and decrease GABA expression. Treatment with IL-1β along with LOS could eliminate the effects of IL-1β. These findings suggest that an interaction between AT1-R and IL-1β in the PVN contributes to progression in HF.
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