ArticleHypertension research : official journal of the Japanese Society of Hypertension2018
Upregulation of Nav1.6 expression in the rostral ventrolateral medulla of stress-induced hypertensive rats.
Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Small-Conductance CaNeuroscience bulletin · 2026Review
- Central Sympathetic Nerve Activation-Mediated Hypertension: Target Mechanisms and Multimodal Interventions-From Basic Research to Clinical Translation.International journal of molecular sciences · 2026Review
- A neural perspective on the treatment of hypertension: the neurological network excitation and inhibition (E/I) imbalance in hypertension.Frontiers in cardiovascular medicine · 2024Review
- CircRNA Galntl6 sponges miR-335 to ameliorate stress-induced hypertension through upregulating Lig3 in rostral ventrolateral medulla.Redox biology · 2023Article
- LncRNA INPP5F ameliorates stress-induced hypertension via the miR-335/Cttn axis in rostral ventrolateral medulla.CNS neuroscience & therapeutics · 2023Article
- Microglia-derived TNF-α contributes to RVLM neuronal mitochondrial dysfunction via blocking the AMPK-Sirt3 pathway in stress-induced hypertension.Journal of neuroinflammation · 2023Article
- Review
- CaMKII enhances voltage-gated sodium channel Nav1.6 activity and neuronal excitability.The Journal of biological chemistry · 2020Article
- Microglia-Derived NLRP3 Activation Mediates the Pressor Effect of Prorenin in the Rostral Ventrolateral Medulla of Stress-Induced Hypertensive Rats.Neuroscience bulletin · 2020Article
- Nav1.6 in the vasomotor center is a promising key molecule in the pathophysiology of stress-induced hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
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8 authors.
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Abstract
The rostral ventrolateral medulla (RVLM) plays a key role in mediating the development of stress-induced hypertension (SIH) by excitation and/or inhibition of sympathetic preganglionic neurons. The voltage-gated sodium channel Nav1.6 has been found to contribute to neuronal hyperexcitability. To examine the expression of Nav1.6 in the RVLM during SIH, a rat model was established by administering electric foot-shocks and noises. We found that Nav1.6 protein expression in the RVLM of SIH rats was higher than that of control rats, peaking at the tenth day of stress. Furthermore, we observed changes in blood pressure correlating with days of stress, with systolic blood pressure (SBP) found to reach a similarly timed peak at the tenth day of stress. Percentages of cells exhibiting colocalization of Nav1.6 with NeuN, a molecular marker of neurons, indicated a strong correlation between upregulation of Nav1.6 expression in NeuN-positive cells and SBP. The level of RSNA was significantly increased after 10 days of stress induction than control group. Compared with the SIHR, knockdown of Nav1.6 in RVLM of the SIHR decreased the level of SBP, heart rate (HR) and renal sympathetic nerve activity (RSNA). These results suggest that upregulated Nav1.6 expression within neurons in the RVLM of SIH rats may contribute to overactivation of the sympathetic system in response to SIH development.
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