ArticleHypertension (Dallas, Tex. : 1979)2019
Activation of ADAM17 (A Disintegrin and Metalloprotease 17) on Glutamatergic Neurons Selectively Promotes Sympathoexcitation.
Article in Hypertension (Dallas, Tex. : 1979), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- ADAM17 Supports Disinhibition of Pre-sympathetic Glutamatergic Neurons Through Microglial Chemotaxis.Neuroscience bulletin · 2026Article
- Targeting Kinin B1R Attenuates Hypertension Through AT1R-Dependent Mechanisms.Circulation research · 2025Article
- Angiotensin-Converting Enzyme-2 (ACE2) Downregulation During Coronavirus Infection.Molecular biotechnology · 2025Review
- New Approaches Targeting the Renin-Angiotensin System: Inhibition of Brain Aminopeptidase A, ACE2 Ubiquitination, and Angiotensinogen.The Canadian journal of cardiology · 2023Review
- SARS-CoV-2 and Hypertension: Evidence Supporting Invasion into the Brain Via Baroreflex Circuitry and the Role of Imbalanced Renin-Angiotensin-Aldosterone-System.Neuroscience insights · 2023Article
- AT1 Receptors: Their Actions from Hypertension to Cognitive Impairment.Cardiovascular toxicology · 2022Review
- Reducing brain TACE activity improves neuroinflammation and cardiac function in heart failure rats.Frontiers in physiology · 2022Article
- ADAM17 Mediates Proteolytic Maturation of Voltage-Gated Calcium Channel Auxiliary αFunction (Oxford, England) · 2022Article
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- Article
- Sympathetic innervation of the mouse kidney and liver arising from prevertebral ganglia.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Implications of ADAM17 activation for hyperglycaemia, obesity and type 2 diabetes.Bioscience reports · 2021Review
- Use of chlorisondamine to assess the neurogenic contribution to blood pressure in mice: An evaluation of method.Physiological reports · 2021Article
- Epigenetic modifications of the renin-angiotensin system in cardiometabolic diseases.Clinical science (London, England : 1979) · 2021Review
- Activation of Kinin B1R Upregulates ADAM17 and Results in ACE2 Shedding in Neurons.International journal of molecular sciences · 2020Article
- Brain angiotensin converting enzyme-2 in central cardiovascular regulation.Clinical science (London, England : 1979) · 2020Review
- Brain Testosterone-CYP1B1 (Cytochrome P450 1B1) Generated Metabolite 6β-Hydroxytestosterone Promotes Neurogenic Hypertension and Inflammation.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Interactions of the Brain Renin-Angiotensin-System (RAS) and Inflammation in the Sensitization of Hypertension.Frontiers in neuroscience · 2020Review
- ADAM17-Mediated Shedding of Inflammatory Cytokines in Hypertension.Frontiers in pharmacology · 2020Review
- ACE2 and ADAM17 Interaction Regulates the Activity of Presympathetic Neurons.Hypertension (Dallas, Tex. : 1979) · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic activation of the brain renin-angiotensin system contributes to the development of hypertension by altering autonomic balance. Beyond the essential role of Ang II (angiotensin II) type 1 receptors, ADAM17 (A disintegrin and metalloprotease 17) is also found to promote brain renin-angiotensin system overactivation. ADAM17 is robustly expressed in various cell types within the central nervous system. The aim of this study was to determine whether ADAM17 modulates presympathetic neuronal activity to promote autonomic dysregulation in salt-sensitive hypertension. To test our hypothesis, ADAM17 was selectively knocked down in glutamatergic neurons using Cre-loxP technology. In mice lacking ADAM17 in glutamatergic neurons, the blood pressure increase induced by deoxycorticosterone acetate-salt treatment was blunted. Deoxycorticosterone acetate-salt significantly elevated cardiac and vascular sympathetic drive in control mice, while such effects were reduced in mice with ADAM17 knockdown. This blunted sympathoexcitation was extended to the spleen, with a lesser activation of the peripheral immune system, translating into a sequestration of circulating T cells within this organ, compared with controls. Within the paraventricular nucleus, Ang II-induced activation of kidney-related presympathetic glutamatergic neurons was reduced in ADAM17 knockdown mice, with the majority of cells no longer responding to Ang II stimulation, confirming the supportive role of ADAM17 in increasing presympathetic neuronal activity. Overall, our data highlight the pivotal role of neuronal ADAM17 in regulating sympathetic activity and demonstrate that activation of ADAM17 in glutamatergic neurons leads to a selective increase of sympathetic output, but not vagal tone, to specific organs, ultimately contributing to dysautonomia and salt-sensitive hypertension.
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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.