| Decreased cardiac Ang-(1-7) is associated with salt-induced cardiac remodeling and dysfunction. | |
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MedLine Citation:
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PMID: 19946038 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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). |
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Authors:
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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:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-11-27 |
Journal Detail:
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Title: Therapeutic advances in cardiovascular disease Volume: 4 ISSN: 1753-9455 ISO Abbreviation: Ther Adv Cardiovasc Dis Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-01-15 Completed Date: 2010-03-25 Revised Date: 2011-09-22 |
Medline Journal Info:
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Nlm Unique ID: 101316343 Medline TA: Ther Adv Cardiovasc Dis Country: England |
Other Details:
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Languages: eng Pagination: 17-25 Citation Subset: IM |
Affiliation:
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Hypertension and Vascular Research Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA. jvaragic@wfubmc.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin I
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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:
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HL-51952/HL/NHLBI NIH HHS; K08 AG026764-04/AG/NIA NIH HHS; KO8-AG026764-04/AG/NIA NIH HHS |
| Chemical | |
Reg. No./Substance:
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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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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