Document Detail


Decreased cardiac Ang-(1-7) is associated with salt-induced cardiac remodeling and dysfunction.
MedLine Citation:
PMID:  19946038     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Angiotensin II has a critical role in the regulation of blood pressure and cell growth and excess activity of the peptide is implicated in the pathogenesis of salt-induced cardiovascular injury. On the other hand, the role of counteracting angiotensin-(1-7) in cardiac structural and functional responses to high salt diet has not been elucidated. Therefore, the present study examined the changes in cardiac angiotensin-(1-7), its forming enzyme angiotensin converting enzyme 2 (ACE2) and receptor mas in response to a high salt diet in spontaneously hypertensive rats (SHR).
METHODS: Eight-week-old male spontaneously hypertensive rats (SHR) were given an 8% salt diet for 5 weeks (n = 8). Age- and gender-matched controls received standard chow (n = 6).
RESULTS: Salt excess increased arterial pressure (p < 0.05) and plasma renin and angiotensin II concentrations (p < 0.05). Salt-induced left ventricular remodeling and diastolic dysfunction were associated with diminished levels of angiotensin-(1-7) in the heart (p < 0.05) and no changes in cardiac angiotensin II levels. Exposure to high salt intake decreased cardiac ACE2 mRNA and protein level (p < 0.05). There was no difference in the protein levels of angiotensin II type 1 and mas receptors between the two experimental groups.
CONCLUSION: The adverse cardiac effects of excessive salt intake may result not only from the undesirable action of angiotensin II but may also be a consequence of diminished protective effects of the angiotensin-(1-7).
Authors:
Jasmina Varagic; Sarfaraz Ahmad; K Bridget Brosnihan; Leanne Groban; Mark C Chappell; E Ann Tallant; Patricia E Gallagher; Carlos M Ferrario
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-11-27
Journal Detail:
Title:  Therapeutic advances in cardiovascular disease     Volume:  4     ISSN:  1753-9455     ISO Abbreviation:  Ther Adv Cardiovasc Dis     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-01-15     Completed Date:  2010-03-25     Revised Date:  2013-08-26    
Medline Journal Info:
Nlm Unique ID:  101316343     Medline TA:  Ther Adv Cardiovasc Dis     Country:  England    
Other Details:
Languages:  eng     Pagination:  17-25     Citation Subset:  IM    
Affiliation:
Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA. jvaragic@wfubmc.edu
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MeSH Terms
Descriptor/Qualifier:
Angiotensin I / metabolism*
Angiotensin II / blood
Animals
Blood Pressure
Male
Peptide Fragments / metabolism*
Peptidyl-Dipeptidase A / genetics,  metabolism
Proto-Oncogene Proteins / metabolism
RNA, Messenger / metabolism
Rats
Rats, Inbred SHR
Receptors, G-Protein-Coupled / metabolism
Renin / blood
Sodium Chloride, Dietary / toxicity*
Ventricular Dysfunction, Left / etiology*
Ventricular Remodeling*
Grant Support
ID/Acronym/Agency:
HL-51952/HL/NHLBI NIH HHS; K08 AG026764-04/AG/NIA NIH HHS; KO8-AG026764-04/AG/NIA NIH HHS; R01 AG033727/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Peptide Fragments; 0/Proto-Oncogene Proteins; 0/RNA, Messenger; 0/Receptors, G-Protein-Coupled; 0/Sodium Chloride, Dietary; 0/angiotensin I (1-7); 0/proto-oncogene proteins c-mas-1; 11128-99-7/Angiotensin II; 9041-90-1/Angiotensin I; EC 3.4.15.1/Peptidyl-Dipeptidase A; EC 3.4.17.-/angiotensin converting enzyme 2; EC 3.4.23.15/Renin
Comments/Corrections

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


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