Document Detail


Macrophage migration inhibitory factor in the nucleus of solitary tract decreases blood pressure in SHRs.
MedLine Citation:
PMID:  22997157     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS: The macrophage migration inhibitory factor (MIF) is an intracellular inhibitor of the central nervous system actions of angiotensin II on blood pressure. Considering that angiotensin II actions at the nucleus of the solitary tract are important for the maintenance of hypertension in spontaneously hypertensive rats (SHRs), we tested if increased MIF expression in the nucleus of the solitary tract of SHR alters the baseline high blood pressure in these rats.
METHODS AND RESULTS: Eight-week-old SHRs or normotensive rats were microinjected with the vector AAV2-CBA-MIF into the nucleus of the solitary tract, resulting in MIF expression predominantly in neurons. Rats also underwent recordings of the mean arterial blood pressure (MAP) and heart rate (via telemetry devices implanted in the abdominal aorta), cardiac- and baroreflex function. Injections of AAV2-CBA-MIF into the nucleus of the solitary tract of SHRs produced significant decreases in the MAP, ranging from 10 to 20 mmHg, compared with age-matched SHRs that had received identical microinjections of the control vector AAV2-CBA-eGFP. This lowered MAP in SHRs was maintained through the end of the experiment at 31 days, and was associated with an improvement in baroreflex function to values observed in normotensive rats. In contrast to SHRs, similar increased MIF expression in the nucleus of the solitary tract of normotensive rats produced no changes in baseline MAP and baroreflex function.
CONCLUSION: These results indicate that an increased expression of MIF within the nucleus of the solitary tract neurons of SHRs lowers blood pressure and restores baroreflex function.
Authors:
André Henrique Freiria-Oliveira; Graziela Torres Blanch; Hongwei Li; Eduardo Colombari; Débora Simões Almeida Colombari; Colin Sumners
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-09-20
Journal Detail:
Title:  Cardiovascular research     Volume:  97     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2012-12-24     Completed Date:  2013-06-03     Revised Date:  2014-01-09    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  153-60     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Arterial Pressure*
Baroreflex
Cardiomegaly / metabolism,  physiopathology
Dependovirus / genetics
Disease Models, Animal
Genetic Therapy*
Genetic Vectors
Heart Rate
Hypertension / genetics,  metabolism,  physiopathology,  therapy*
Intramolecular Oxidoreductases / genetics,  metabolism
Macrophage Migration-Inhibitory Factors / genetics,  metabolism*
Male
Microinjections
RNA, Messenger / metabolism
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Solitary Nucleus / metabolism*,  physiopathology
Telemetry
Time Factors
Ventricular Function, Left
Grant Support
ID/Acronym/Agency:
HL-076803/HL/NHLBI NIH HHS; HL-093186/HL/NHLBI NIH HHS; R01 HL076803/HL/NHLBI NIH HHS; R01 HL093186/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Macrophage Migration-Inhibitory Factors; 0/RNA, Messenger; EC 5.3.-/Intramolecular Oxidoreductases; EC 5.3.2.1/Mif protein, rat
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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