Document Detail


Intratubular Renin-Angiotensin System in Hypertension.
MedLine Citation:
PMID:  19789728     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
It is well recognized that the renin-angiotensin system plays an important role in the regulation of arterial pressure and sodium homeostasis. Recent years, many studies have shown that local tissue angiotensin II levels are differentially regulated and cannot be explained on the basis of circulating concentrations. All of the components needed for angiotensin II generation are present within the various compartments in the kidney including the renal interstitium and the tubular network. The cascade of the renin-angiotensin system demonstrates three major possible sites for the pharmacological interruption of the renin-angiotensin system: the interaction of renin with its substrate, angiotensinogen, the angiotensin converting enzyme, and angiotensin II type 1 receptors. This brief article will focus on the role of the intratubular renin-angiotensin system in the pathophysiology of hypertension and the responses to the renin-angiotensin system blockade by renin inhibitors, angiotensin converting enzyme inhibitors and angiotensin II type 1 receptor blockers.
Authors:
Yuki Suzaki; Minolfa C Prieto-Carrasquero; Hiroyuki Kobori
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Publication Detail:
Type:  JOURNAL ARTICLE    
Journal Detail:
Title:  Current hypertension reviews     Volume:  2     ISSN:  1875-6506     ISO Abbreviation:  -     Publication Date:  2006  
Date Detail:
Created Date:  2010-8-16     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101239891     Medline TA:  Curr Hypertens Rev     Country:  -    
Other Details:
Languages:  ENG     Pagination:  151-157     Citation Subset:  -    
Affiliation:
Department of Physiology, and Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, LA, USA.
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Descriptor/Qualifier:
Grant Support
ID/Acronym/Agency:
R01 DK072408-01A1//NIDDK NIH HHS; R01 DK072408-01A1//NIDDK NIH HHS

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