Document Detail


The role of renal microvascular disease and interstitial inflammation in salt-sensitive hypertension.
MedLine Citation:
PMID:  20686485     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Primary (essential) hypertension has been shown to be mediated by a relative impairment in sodium excretion by the kidney, but the mechanisms responsible for this defect are still being clarified. Increasing evidence suggests a role for subtle acquired renal injury in mediating this process. Microvascular injury is present in the majority of subjects with hypertension. The development of arteriolosclerosis, primarily of the afferent arteriole, may interfere with glomerular autoregulation, whereas the loss of peritubular capillaries may facilitate local ischemia. These changes favor the localization of T cells and macrophages into the interstitium, which, coupled with local oxidative stress and angiotensin II generation, may contribute to the impaired pressure natriuresis observed with salt-sensitive hypertension. Consistent with this hypothesis, therapies that are aimed at blocking the immune response, including thymectomy, genetic alterations in mice resulting in impaired immune responses, or the use of immunosuppressive agents, can protect against the development of hypertension in experimental models. Preliminary data in humans also suggest that the inhibition of the renal inflammatory response may reduce blood pressure. The present investigations are directed to gain insight in the role of the intrarenal T-cell reactivity and autoimmunity in driving the tubulointerstitial inflammation and its participation in the pathogenesis of salt-sensitive hypertension.
Authors:
Bernardo Rodriguez-Iturbe; Richard J Johnson
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Publication Detail:
Type:  Journal Article; Review     Date:  2010-08-05
Journal Detail:
Title:  Hypertension research : official journal of the Japanese Society of Hypertension     Volume:  33     ISSN:  1348-4214     ISO Abbreviation:  Hypertens. Res.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-05     Completed Date:  2011-02-01     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9307690     Medline TA:  Hypertens Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  975-80     Citation Subset:  IM    
Affiliation:
Hospital Universitario and Universidad del Zulia, IVIC-Zulia, Maracaibo, Venezuela. bernardori@telcel.net.ve
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MeSH Terms
Descriptor/Qualifier:
Animals
HSP72 Heat-Shock Proteins / physiology
Humans
Hypertension / physiopathology*
Kidney Diseases / physiopathology*
Mice
Microvessels / physiopathology
Models, Animal
Natriuresis / physiology
Nephritis, Interstitial / physiopathology*
Oxidative Stress / physiology
Chemical
Reg. No./Substance:
0/HSP72 Heat-Shock Proteins

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


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