Document Detail


Down-regulation of basal Fos expression at nucleus tractus solitarii underlies restoration of baroreflex response after antihypertensive treatment in spontaneously hypertensive rats.
MedLine Citation:
PMID:  12044476     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Antihypertensive therapy not only normalizes the elevated blood pressure but also restores the reduced baroreceptor reflex response associated with hypertension, although the underlying mechanism is not fully understood. We assessed the hypothesis that a reversal of the enhanced basal Fos expression seen during hypertension in nucleus tractus solitarii, the terminal site of baroreceptor afferents, underlies the restoration of baroreceptor reflex sensitivity after antihypertensive treatment. Male adult spontaneously hypertensive or normotensive Wistar-Kyoto rats received for 3 weeks captopril (100 mg/kg/day) added to their drinking water. Evaluated subsequently under pentobarbital anesthesia, captopril-treated spontaneously hypertensive rats exhibited significantly lowered systolic blood pressure and restoration of the sensitivity in baroreceptor reflex control of heart rate to levels comparable with Wistar-Kyoto rats. Reverse transcription-polymerase chain reaction analysis and immunohistochemical evaluation revealed concomitant down-regulation of basal expression in nucleus tractus solitarii of c-fos gene at both mRNA and protein levels. Captopril treatment, on the other hand, elicited no discernible effect on systolic blood pressure, cardiac baroreceptor reflex sensitivity or basal expression of Fos protein at the nucleus tractus solitarii of normotensive Wistar-Kyoto rats. From these findings we suggest that a down-regulation of basal Fos expression in nucleus tractus solitarii may contribute to the restoration of baroreceptor reflex sensitivity in spontaneously hypertensive rats that received antihypertensive treatment such as captopril.
Authors:
S H H Chan; Y M Chao; C J Tseng; J Y H Chan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Neuroscience     Volume:  112     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2002  
Date Detail:
Created Date:  2002-06-04     Completed Date:  2002-09-06     Revised Date:  2009-11-03    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  113-20     Citation Subset:  IM    
Affiliation:
Neuroscience Group, Chang Gung University and Kaohsiung Chang Gung Memorial Hospital, Taiwan, Republic of China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antihypertensive Agents / pharmacology*
Baroreflex / drug effects*
Blood Pressure / drug effects
Captopril / pharmacology*
Down-Regulation
Hypertension / metabolism*,  physiopathology
Immunohistochemistry
Male
Proto-Oncogene Proteins c-fos / metabolism*
RNA, Messenger / metabolism
Rats
Rats, Inbred SHR / metabolism*
Rats, Inbred WKY
Reference Values
Reverse Transcriptase Polymerase Chain Reaction
Solitary Nucleus / metabolism*
Systole
Chemical
Reg. No./Substance:
0/Antihypertensive Agents; 0/Proto-Oncogene Proteins c-fos; 0/RNA, Messenger; 62571-86-2/Captopril

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