Upregulation of Nav1.6 expression in the rostral ventrolateral medulla of stress-induced hypertensive rats
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 exa...
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Published in | Hypertension research Vol. 41; no. 12; pp. 1013 - 1022 |
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Main Authors | , , , , , , , |
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Language | English |
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Nature Publishing Group
01.12.2018
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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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AbstractList | 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. |
Author | Chen, Qing-Hui Du, Dong-Shu Chen, Fu-Xue Li, Min Wu, Jia-Xiang Tong, Lei Xia, Chun-Mei Hu, Li |
Author_xml | – sequence: 1 givenname: Jia-Xiang surname: Wu fullname: Wu, Jia-Xiang organization: Shanghai Key Laboratory of Bio-Crops, College of Life Science, Shanghai University, Shanghai, China – sequence: 2 givenname: Lei surname: Tong fullname: Tong, Lei organization: Shanghai Key Laboratory of Bio-Crops, College of Life Science, Shanghai University, Shanghai, China – sequence: 3 givenname: Li surname: Hu fullname: Hu, Li organization: Shanghai Key Laboratory of Bio-Crops, College of Life Science, Shanghai University, Shanghai, China – sequence: 4 givenname: Chun-Mei surname: Xia fullname: Xia, Chun-Mei organization: Department of Physiology and Pathophysiology, Shanghai Medical College of Fudan University, Shanghai, China – sequence: 5 givenname: Min surname: Li fullname: Li, Min organization: Shanghai Key Laboratory of Bio-Crops, College of Life Science, Shanghai University, Shanghai, China – sequence: 6 givenname: Qing-Hui surname: Chen fullname: Chen, Qing-Hui organization: Department of Kinesiology and Integrative Physiology, Michigan Technological University, Houghton, MI, USA – sequence: 7 givenname: Fu-Xue surname: Chen fullname: Chen, Fu-Xue organization: Shanghai Key Laboratory of Bio-Crops, College of Life Science, Shanghai University, Shanghai, China – sequence: 8 givenname: Dong-Shu surname: Du fullname: Du, Dong-Shu email: sdhzdds@163.com organization: Shanghai Key Laboratory of Bio-Crops, College of Life Science, Shanghai University, Shanghai, China. sdhzdds@163.com |
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SubjectTerms | Animals Antigens, Nuclear - metabolism Blood pressure Hypertension Hypertension - etiology Hypertension - metabolism Kidney - innervation Male Medulla Oblongata - metabolism NAV1.6 Voltage-Gated Sodium Channel - genetics NAV1.6 Voltage-Gated Sodium Channel - metabolism Nerve Tissue Proteins - metabolism Neurons Neurons - metabolism Rats Rats, Sprague-Dawley Rodents Stress, Psychological - complications Stress, Psychological - metabolism Sympathetic Nervous System - metabolism Up-Regulation |
Title | Upregulation of Nav1.6 expression in the rostral ventrolateral medulla of stress-induced hypertensive rats |
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