Microglia Participate in Neurogenic Regulation of Hypertension
Hypertension is associated with neuroinflammation and increased sympathetic tone. Interference with neuroinflammation by an anti-inflammatory reagent or overexpression of interleukin-10 in the brain was found to attenuate hypertension. However, the cellular mechanism of neuroinflammation, as well as...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2015-08, Vol.66 (2), p.309-316 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Shen, Xiao Z Li, You Li, Liang Shah, Kandarp H Bernstein, Kenneth E Lyden, Patrick Shi, Peng |
| description | Hypertension is associated with neuroinflammation and increased sympathetic tone. Interference with neuroinflammation by an anti-inflammatory reagent or overexpression of interleukin-10 in the brain was found to attenuate hypertension. However, the cellular mechanism of neuroinflammation, as well as its impact on neurogenic regulation of blood pressure, is unclear. Here, we found that hypertension, induced by either angiotensin II or L-N-nitro-l-arginine methyl ester, is accompanied by microglial activation as manifested by microgliosis and proinflammatory cytokine upregulation. Targeted depletion of microglia significantly attenuated neuroinflammation, glutamate receptor expression in the paraventricular nucleus, plasma vasopressin level, kidney norepinephrine concentration, and blood pressure. Furthermore, when microglia were preactivated and transferred into the brains of normotensive mice, there was a significantly prolonged pressor response to intracerebroventricular injection of angiotensin II, and inactivation of microglia eliminated these effects. These data demonstrate that microglia, the resident immune cells in the brain, are the major cellular factors in mediating neuroinflammation and modulating neuronal excitation, which contributes to the elevated blood pressure. |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.115.05333 |
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Interference with neuroinflammation by an anti-inflammatory reagent or overexpression of interleukin-10 in the brain was found to attenuate hypertension. However, the cellular mechanism of neuroinflammation, as well as its impact on neurogenic regulation of blood pressure, is unclear. Here, we found that hypertension, induced by either angiotensin II or L-N-nitro-l-arginine methyl ester, is accompanied by microglial activation as manifested by microgliosis and proinflammatory cytokine upregulation. Targeted depletion of microglia significantly attenuated neuroinflammation, glutamate receptor expression in the paraventricular nucleus, plasma vasopressin level, kidney norepinephrine concentration, and blood pressure. Furthermore, when microglia were preactivated and transferred into the brains of normotensive mice, there was a significantly prolonged pressor response to intracerebroventricular injection of angiotensin II, and inactivation of microglia eliminated these effects. 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Interference with neuroinflammation by an anti-inflammatory reagent or overexpression of interleukin-10 in the brain was found to attenuate hypertension. However, the cellular mechanism of neuroinflammation, as well as its impact on neurogenic regulation of blood pressure, is unclear. Here, we found that hypertension, induced by either angiotensin II or L-N-nitro-l-arginine methyl ester, is accompanied by microglial activation as manifested by microgliosis and proinflammatory cytokine upregulation. Targeted depletion of microglia significantly attenuated neuroinflammation, glutamate receptor expression in the paraventricular nucleus, plasma vasopressin level, kidney norepinephrine concentration, and blood pressure. Furthermore, when microglia were preactivated and transferred into the brains of normotensive mice, there was a significantly prolonged pressor response to intracerebroventricular injection of angiotensin II, and inactivation of microglia eliminated these effects. These data demonstrate that microglia, the resident immune cells in the brain, are the major cellular factors in mediating neuroinflammation and modulating neuronal excitation, which contributes to the elevated blood pressure.</description><subject>Angiotensin II - adverse effects</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Diphtheria Toxin - administration & dosage</subject><subject>Diphtheria Toxin - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - physiopathology</subject><subject>Infusions, Intraventricular</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microglia - drug effects</subject><subject>Microglia - physiology</subject><subject>NG-Nitroarginine Methyl Ester - adverse effects</subject><subject>Sympathetic Nervous System - physiology</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkN1uEzEQhS1ERUPhFdByx80Wz_pn1zeVoiqQSiWtSpHgypp1JonB2U3tXaq-PYaUqu1I1mhmvjkeHcbeAz8G0PBx_uNydnU9W3w9u1hM59PcVMdcCSFesAmoSpZSafGSTTgYWRqA74fsdUo_OQcpZf2KHVaaZ0KYCTv54l3s18FjcYlx8M7vcKDCd8WCxjygzrviitZjwMH3XdGvivndjuJAXcr1G3awwpDo7X0-Yt8-za5P5-X5xeez0-l56ZThdemEg5pjoxrdgmtaatsKWw1tPmhpjOHLGlEtqdUCRYUGJPIGVoq0q4AkiCN2stfdje2Wlo66IWKwu-i3GO9sj94-nXR-Y9f9byulaYyWWeDDvUDsb0ZKg9365CgE7KgfkwVtFDRaCZ1Rs0ezMSlFWj18A9z-9d8-8z83lf3nf9599_jOh83_hmdA7oHbPgwU068w3lK0G8IwbCzPISvdlBUHxZtclflBLf4AaXWUYg</recordid><startdate>201508</startdate><enddate>201508</enddate><creator>Shen, Xiao Z</creator><creator>Li, You</creator><creator>Li, Liang</creator><creator>Shah, Kandarp H</creator><creator>Bernstein, Kenneth E</creator><creator>Lyden, Patrick</creator><creator>Shi, Peng</creator><general>American Heart Association, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201508</creationdate><title>Microglia Participate in Neurogenic Regulation of Hypertension</title><author>Shen, Xiao Z ; Li, You ; Li, Liang ; Shah, Kandarp H ; Bernstein, Kenneth E ; Lyden, Patrick ; Shi, Peng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5907-c3c170a8586b1c8bebb2ab61b144d9990d7aa5deb63a32a914a081f5e6c21e413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Angiotensin II - adverse effects</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Diphtheria Toxin - administration & dosage</topic><topic>Diphtheria Toxin - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - physiopathology</topic><topic>Infusions, Intraventricular</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microglia - drug effects</topic><topic>Microglia - physiology</topic><topic>NG-Nitroarginine Methyl Ester - adverse effects</topic><topic>Sympathetic Nervous System - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shen, Xiao Z</creatorcontrib><creatorcontrib>Li, You</creatorcontrib><creatorcontrib>Li, Liang</creatorcontrib><creatorcontrib>Shah, Kandarp H</creatorcontrib><creatorcontrib>Bernstein, Kenneth E</creatorcontrib><creatorcontrib>Lyden, Patrick</creatorcontrib><creatorcontrib>Shi, Peng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shen, Xiao Z</au><au>Li, You</au><au>Li, Liang</au><au>Shah, Kandarp H</au><au>Bernstein, Kenneth E</au><au>Lyden, Patrick</au><au>Shi, Peng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Microglia Participate in Neurogenic Regulation of Hypertension</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2015-08</date><risdate>2015</risdate><volume>66</volume><issue>2</issue><spage>309</spage><epage>316</epage><pages>309-316</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><abstract>Hypertension is associated with neuroinflammation and increased sympathetic tone. Interference with neuroinflammation by an anti-inflammatory reagent or overexpression of interleukin-10 in the brain was found to attenuate hypertension. However, the cellular mechanism of neuroinflammation, as well as its impact on neurogenic regulation of blood pressure, is unclear. Here, we found that hypertension, induced by either angiotensin II or L-N-nitro-l-arginine methyl ester, is accompanied by microglial activation as manifested by microgliosis and proinflammatory cytokine upregulation. Targeted depletion of microglia significantly attenuated neuroinflammation, glutamate receptor expression in the paraventricular nucleus, plasma vasopressin level, kidney norepinephrine concentration, and blood pressure. Furthermore, when microglia were preactivated and transferred into the brains of normotensive mice, there was a significantly prolonged pressor response to intracerebroventricular injection of angiotensin II, and inactivation of microglia eliminated these effects. 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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Angiotensin II - adverse effects Animals Apoptosis - drug effects Blood Pressure - physiology Diphtheria Toxin - administration & dosage Diphtheria Toxin - pharmacology Disease Models, Animal Hypertension - chemically induced Hypertension - physiopathology Infusions, Intraventricular Mice Mice, Inbred C57BL Microglia - drug effects Microglia - physiology NG-Nitroarginine Methyl Ester - adverse effects Sympathetic Nervous System - physiology |
| title | Microglia Participate in Neurogenic Regulation of Hypertension |
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