ArticleNeural plasticity2017
Enhancement in Tonically Active Glutamatergic Inputs to the Rostral Ventrolateral Medulla Contributes to Neuropathic Pain-Induced High Blood Pressure.
Article in Neural plasticity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Electroacupuncture Regulates Sympathetic Nerve Through the NTSCNS neuroscience & therapeutics · 2025Article
- Inhibition of NMDA Receptor Activation in the Rostral Ventrolateral Medulla by Amyloid-β Peptide in Rats.Biomolecules · 2023Article
- DPP3: From biomarker to therapeutic target of cardiovascular diseases.Frontiers in cardiovascular medicine · 2022Review
- Effect of the Non-N-Methyl-D-aspartate Receptor of the Glutamatergic System of the Pedunculopontine Tegmental Nucleus on Cardiovascular Responses in Normotensive and Hydralazine-Induced Hypotensive Rats.Advanced biomedical research · 2022Article
- Upregulating Nrf2 in the RVLM ameliorates sympatho-excitation in mice with chronic heart failure.Free radical biology & medicine · 2019Article
- Combined hyperactive dysfunction syndrome of the cranial nerves complicated by essential hypertension: A case report.Medicine · 2019Article
- Angiotensin-Converting Enzyme 2 in the Rostral Ventrolateral Medulla Regulates Cholinergic Signaling and Cardiovascular and Sympathetic Responses in Hypertensive Rats.Neuroscience bulletin · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain increases the risk of cardiovascular diseases including hypertension with the characteristic of sympathetic overactivity. The enhanced tonically active glutamatergic input to the rostral ventrolateral medulla (RVLM) contributes to sympathetic overactivity and blood pressure (BP) in cardiovascular diseases. We hypothesize that neuropathic pain enhances tonically active glutamatergic inputs to the RVLM, which contributes to high level of BP and sympathetic outflow. Animal model with the trigeminal neuropathic pain was induced by the infraorbital nerve-chronic constriction injury (ION-CCI). A significant increase in BP and renal sympathetic nerve activity (RSNA) was found in rats with ION-CCI (BP,
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