| The ANG-(1-7)/ACE2/mas axis in the regulation of nephron function. | |
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MedLine Citation:
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PMID: 20375118 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The study of experimental hypertension and the development of drugs with selective inhibitory effects on the enzymes and receptors constituting the components of the circulating and tissue renin-angiotensin systems have led to newer concepts of how this system participates in both physiology and pathology. Over the last decade, a renewed emphasis on understanding the role of angiotensin-(1-7) and angiotensin-converting enzyme 2 in the regulation of blood pressure and renal function has shed new light on the complexity of the mechanisms by which these components of the renin angiotensin system act in the heart and in the kidneys to exert a negative regulatory influence on angiotensin converting enzyme and angiotensin II. The vasodepressor axis composed of angiotensin-(1-7)/angiotensin-converting enzyme 2/mas receptor emerges as a site for therapeutic interventions within the renin-angiotensin system. This review summarizes the evolving knowledge of the counterregulatory arm of the renin-angiotensin system in the control of nephron function and renal disease. |
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Authors:
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Carlos M Ferrario; Jasmina Varagic |
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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; Review Date: 2010-04-07 |
Journal Detail:
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Title: American journal of physiology. Renal physiology Volume: 298 ISSN: 1522-1466 ISO Abbreviation: Am. J. Physiol. Renal Physiol. Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-05-21 Completed Date: 2010-06-14 Revised Date: 2011-07-28 |
Medline Journal Info:
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Nlm Unique ID: 100901990 Medline TA: Am J Physiol Renal Physiol Country: United States |
Other Details:
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Languages: eng Pagination: F1297-305 Citation Subset: IM |
Affiliation:
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Hypertension and Vascular Disease Research Center and Department of Surgery, Wake Forest University School of Medicine, Winston Salem, North Carolina 27157, USA. cferrari@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 / metabolism* Animals Antihypertensive Agents / therapeutic use Blood Pressure Humans Hypertension / drug therapy, enzymology*, physiopathology Nephrons / drug effects, enzymology*, physiopathology Peptide Fragments / metabolism* Peptidyl-Dipeptidase A / metabolism* Proto-Oncogene Proteins / metabolism* Receptors, G-Protein-Coupled / metabolism* Signal Transduction* / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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P01 HL051952/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antihypertensive Agents; 0/Peptide Fragments; 0/Proto-Oncogene Proteins; 0/Receptors, G-Protein-Coupled; 0/angiotensin I (1-7); 0/proto-oncogene proteins c-mas-1; 11128-99-7/Angiotensin II; 51833-78-4/angiotensin II (1-7); 9041-90-1/Angiotensin I; EC 3.4.15.1/Peptidyl-Dipeptidase A; EC 3.4.17.-/angiotensin converting enzyme 2 |
| Comments/Corrections | |
Erratum In:
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Am J Physiol Renal Physiol. 2010 Dec;299(6):F1515 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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