| Central and peripheral mechanisms of T-lymphocyte activation and vascular inflammation produced by angiotensin II-induced hypertension. | |
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MedLine Citation:
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PMID: 20558826 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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RATIONALE: We have previously found that T lymphocytes are essential for development of angiotensin II-induced hypertension; however, the mechanisms responsible for T-cell activation in hypertension remain undefined. OBJECTIVE: We sought to study the roles of the CNS and pressure elevation in T-cell activation and vascular inflammation caused by angiotensin II. METHODS AND RESULTS: To prevent the central actions of angiotensin II, we created anteroventral third cerebral ventricle (AV3V) lesions in mice. The elevation in blood pressure in response to angiotensin II was virtually eliminated by AV3V lesions, as was activation of circulating T cells and the vascular infiltration of leukocytes. In contrast, AV3V lesioning did not prevent the hypertension and T-cell activation caused by the peripheral acting agonist norepinephrine. To determine whether T-cell activation and vascular inflammation are attributable to central influences or are mediated by blood pressure elevation, we administered hydralazine (250 mg/L) in the drinking water. Hydralazine prevented the hypertension and abrogated the increase in circulating activated T cells and vascular infiltration of leukocytes caused by angiotensin II. CONCLUSIONS: We conclude that the central and pressor effects of angiotensin II are critical for T-cell activation and development of vascular inflammation. These findings also support a feed-forward mechanism in which modest degrees of blood pressure elevation lead to T-cell activation, which in turn promotes inflammation and further raises blood pressure, leading to severe hypertension. |
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Authors:
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Paul J Marvar; Salim R Thabet; Tomasz J Guzik; Heinrich E Lob; Louise A McCann; Connie Weyand; Frank J Gordon; David G Harrison |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2010-06-17 |
Journal Detail:
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Title: Circulation research Volume: 107 ISSN: 1524-4571 ISO Abbreviation: Circ. Res. Publication Date: 2010 Jul |
Date Detail:
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Created Date: 2010-07-23 Completed Date: 2010-08-24 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: United States |
Other Details:
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Languages: eng Pagination: 263-70 Citation Subset: IM |
Affiliation:
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Division of Cardiology, Emory University School of Medicine, Atlanta, GA 30322, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Administration, Oral Adoptive Transfer Angiotensin II Animals Antihypertensive Agents / administration & dosage Blood Pressure Disease Models, Animal Genes, T-Cell Receptor alpha Genes, T-Cell Receptor beta Homeodomain Proteins / genetics, metabolism Hydralazine / administration & dosage Hypertension / chemically induced, genetics, immunology*, metabolism, physiopathology, prevention & control Lymphocyte Activation* / drug effects Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Norepinephrine Receptors, Antigen, T-Cell, alpha-beta / immunology Superoxides / metabolism T-Lymphocytes / drug effects, immunology*, transplantation Third Ventricle / immunology*, injuries, physiopathology Time Factors Vasculitis / chemically induced, genetics, immunology*, metabolism, physiopathology, prevention & control |
| Grant Support | |
ID/Acronym/Agency:
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EY11916/EY/NEI NIH HHS; HL390006/HL/NHLBI NIH HHS; HL58000/HL/NHLBI NIH HHS; HL59248/HL/NHLBI NIH HHS; HL63919/HL/NHLBI NIH HHS; P01 HL058000-01A10002/HL/NHLBI NIH HHS; P01 HL058000-11A1/HL/NHLBI NIH HHS; R01 HL039006-23/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antihypertensive Agents; 0/Homeodomain Proteins; 0/Receptors, Antigen, T-Cell, alpha-beta; 11062-77-4/Superoxides; 11128-99-7/Angiotensin II; 128559-51-3/RAG-1 protein; 51-41-2/Norepinephrine; 86-54-4/Hydralazine |
| Comments/Corrections | |
Comment In:
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Circ Res. 2010 Jul 23;107(2):166-7
[PMID:
20651292
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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