ArticleOncotarget2016
Renal denervation attenuates aldosterone expression and associated cardiovascular pathophysiology in angiotensin II-induced hypertension.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- Effect of renal denervation on catecholamines and the renin-angiotensin-aldosterone system.Journal of the renin-angiotensin-aldosterone system : JRAASTrial
- Mesenchymal Stem Cells Therapies on Fibrotic Heart Diseases.International journal of molecular sciences · 2021Review
- Efficacy and safety of renal denervation in addition to pulmonary vein isolation for atrial fibrillation and hypertension-Systematic review and meta-analysis of randomized controlled trials.Journal of arrhythmia · 2020Article
- Steroidogenic acute regulatory protein/aldosterone synthase mediates angiotensin II-induced cardiac fibrosis and hypertrophy.Molecular biology reports · 2020Article
- Renal denervation and CD161a immune ablation prevent cholinergic hypertension and renal sodium retention.American journal of physiology. Heart and circulatory physiology · 2019Article
- The renin-angiotensin system in cardiovascular autonomic control: recent developments and clinical implications.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2019Review
- Innate and Innate-Like Immune System in Hypertension and Vascular Injury.Current hypertension reports · 2019Review
- Chronic intermittent hypoxia-mediated renal sympathetic nerve activation in hypertension and cardiovascular disease.Scientific reports · 2018Article
- Association between echocardiographic structural parameters and body weight in Wistar rats.Oncotarget · 2017Article
- A promoter polymorphism in APJ gene is significantly associated with blood pressure changes and hypertension risk in Chinese women.Oncotarget · 2016Article
- Relationship Between 25-Hydroxyvitamin D, Renin, and Collagen Remodeling Biomarkers in Atrial Fibrillation.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
- The role of Mas receptor on renal hemodynamic responses to angiotensin II administration in chronic renal sympathectomized male and female rats.Research in pharmaceutical sciencesArticle
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sympathetic nervous system interacts with the renin-angiotensin-aldosterone system (RAAS) contributing to cardiovascular diseases. In this study, we sought to determine if renal denervation (RDN) inhibits aldosterone expression and associated cardiovascular pathophysiological changes in angiotensin II (Ang II)-induced hypertension. Bilateral RDN or SHAM operation was performed before chronic 14-day Ang II subcutaneous infusion (200ng/kg/min) in male Sprague-Dawley rats. Bilateral RDN blunted Ang II-induced hypertension and ameliorated the mesenteric vascular dysfunction. Cardiovascular hypertrophy in response to Ang II was significantly attenuated by RDN as shown by histopathology and transthoracic echocardiography. Moreover, Ang II-induced vascular and myocardial inflammation and fibrosis were suppressed by RDN with concurrent decrease in fibronectin and collagen deposition, macrophage infiltration, and MCP-1 expression. Interestingly, RDN also inhibited Ang II-induced aldosterone expression in the plasma, kidney and heart. This was associated with the reduction of calcitonin gene-related peptide (CGRP) in the adrenal gland. Ang II promoted aldosterone secretion which was partly attenuated by CGRP in the adrenocortical cell line, suggesting a protective role of CGRP in this model. Activation of transforming growth factor-β (TGF-β)/Smad and mitogen-activated protein kinases (MAPKs) signaling pathway was both inhibited by RDN especially in the heart. These results suggest that the regulation of the renal sympathetic nerve in Ang II-induced hypertension and associated cardiovascular pathophysiological changes is likely mediated by aldosterone, with CGRP involvement.
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