ArticleThe Journal of physiology2014
Mineralocorticoid and AT1 receptors in the paraventricular nucleus contribute to sympathetic hyperactivity and cardiac dysfunction in rats post myocardial infarct.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Inhibition of sympathetic tone via hypothalamic descending pathway propagates glucocorticoid-induced endothelial impairment and osteonecrosis of the femoral head.Bone research · 2024Article
- Vitamin D Deficiency, Chronic Kidney Disease and Periodontitis.Medicina (Kaunas, Lithuania) · 2024Review
- Microglia-Mediated Neuroimmune Response Regulates Cardiac Remodeling After Myocardial Infarction.Journal of the American Heart Association · 2023Article
- Multiple Aspects of Inappropriate Action of Renin-Angiotensin, Vasopressin, and Oxytocin Systems in Neuropsychiatric and Neurodegenerative Diseases.Journal of clinical medicine · 2022Review
- Is RAS the Link Between COVID-19 and Increased Stress in Head and Neck Cancer Patients?Frontiers in cell and developmental biology · 2021Review
- Counter-regulatory renin-angiotensin system in cardiovascular disease.Nature reviews. Cardiology · 2020Review
- Endogenous AT1 receptor-protein kinase C activity in the hypothalamus augments glutamatergic input and sympathetic outflow in hypertension.The Journal of physiology · 2019Article
- Mineralocorticoid receptor deficiency improves the therapeutic effects of mesenchymal stem cells for myocardial infarction via enhanced cell survival.Journal of cellular and molecular medicine · 2019Article
- Sex differences in the central and peripheral manifestations of ischemia-induced heart failure in rats.American journal of physiology. Heart and circulatory physiology · 2019Article
- Angiotensin II Type 1a Receptors in the Subfornical Organ Modulate Neuroinflammation in the Hypothalamic Paraventricular Nucleus in Heart Failure Rats.Neuroscience · 2018Article
- Activation of oxytocin neurons in the paraventricular nucleus drives cardiac sympathetic nerve activation following myocardial infarction in rats.Communications biology · 2018Article
- Promise of adeno-associated virus as a gene therapy vector for cardiovascular diseases.Heart failure reviews · 2017Review
- TNF-α receptor 1 knockdown in the subfornical organ ameliorates sympathetic excitation and cardiac hemodynamics in heart failure rats.American journal of physiology. Heart and circulatory physiology · 2017Article
- Update on angiotensin II: new endocrine connections between the brain, adrenal glands and the cardiovascular system.Endocrine connections · 2017Review
- How Is the Brain Renin-Angiotensin System Regulated?Hypertension (Dallas, Tex. : 1979) · 2017Review
- Adeno-associated virus-mediated gene therapy in cardiovascular disease.Current opinion in cardiology · 2015Review
- Article
- Taurine Supplementation Ameliorates the Adverse Effects of Perinatal Taurine Depletion and High Sugar Intake on Cardiac Ischemia/Reperfusion Injury of Adult Female Rats.Advances in experimental medicine and biologyArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Intracerebroventricular infusion of a mineralocorticoid receptor (MR) or angiotensin II type 1 receptor (AT1R) blocker in rats attenuates sympathetic hyperactivity and progressive left ventricular (LV) dysfunction post myocardial infarction (MI). The present study examined whether knockdown of MRs or AT1Rs specifically in the paraventricular nucleus (PVN) contributes to these effects, and compared cardiac effects with those of systemic treatment with the β1-adrenergic receptor blocker metoprolol. The PVN of rats was infused with adeno-associated virus carrying small interfering RNA against either MR (AAV-MR-siRNA) or AT1R (AAV-AT1R-siRNA), or as control scrambled siRNA. At 4 weeks post MI, AT1R but not MR expression was increased in the PVN, excitatory renal sympathetic nerve activity and pressor responses to air stress were enhanced, and arterial baroreflex function was impaired; LV end-diastolic pressure (LVEDP) was increased and LV peak systolic pressure (LVPSP), ejection fraction (EF) and dP/dtmax decreased. AAV-MR-siRNA and AAV-AT1R-siRNA both normalized AT1R expression in the PVN, similarly ameliorated sympathetic and pressor responses to air stress, largely prevented baroreflex desensitization, and improved LVEDP, EF and dP/dtmax as well as cardiac interstitial (but not perivascular) fibrosis. In a second set of rats, metoprolol at 70 or 250 mg kg(-1) day(-1) in the drinking water for 4 weeks post MI did not improve LV function except for a decrease in LVEDP at the lower dose. These results suggest that in rats MR-dependent upregulation of AT1Rs in the PVN contributes to sympathetic hyperactivity, and LV dysfunction and remodelling post MI. In rats, normalizing MR-AT1R signalling in the PVN is a more effective strategy to improve LV dysfunction post MI than systemic β1 blockade.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.