Document Detail


The ANG-(1-7)/ACE2/mas axis in the regulation of nephron function.
MedLine Citation:
PMID:  20375118     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Carlos M Ferrario; Jasmina Varagic
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2010-04-07
Journal Detail:
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:
Created Date:  2010-05-21     Completed Date:  2010-06-14     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F1297-305     Citation Subset:  IM    
Affiliation:
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
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MeSH Terms
Descriptor/Qualifier:
Angiotensin I / 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:
P01 HL051952/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
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; 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:
Am J Physiol Renal Physiol. 2010 Dec;299(6):F1515

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