Document Detail

Oxidative stress and renal dysfunction in salt-sensitive hypertension.
MedLine Citation:
PMID:  11435744     Owner:  NLM     Status:  MEDLINE    
Hypertension is a risk factor for the development of end-stage renal disease. The mechanisms underlying hypertensive nephropathy are poorly understood. There is evidence, however, that in hypertension there is an accumulation of partially reduced oxygen and its derivatives, known collectively as reactive oxygen species, which may contribute to progressive renal dysfunction. In the present study, we assess the contribution of oxidative stress in the development of salt-dependent hypertensive nephrosclerosis. Going beyond previous end point studies, which inferred renal function either indirectly or only qualitatively, we have determined oxidative stress concurrently with direct and quantitative measurements of renal function (via inulin and p-aminohippuric acid clearances). Moreover, in this time-dependent study, the measurements have been taken under low- as well as high-salt diets. As was expected from previous studies, in the Dahl salt-sensitive rat, a high-salt diet (8% NaCl) resulted in the development of hypertension, in a decreased glomerular filtration rate, and in a decreased renal plasma flow as compared with the normotensive control, the Dahl salt-resistant rat. In addition, however, we found clear evidence for the accumulation of reactive oxygen species in renal tissue homogenates of Dahl salt-sensitive rats on the high-salt diet. Our time-dependent protocol also indicated that renal oxidative stress follows, in time, the development of hypertension. We also found that after 2 weeks of increased salt loading, Dahl salt-sensitive rats excreted less cyclic guanosine monophosphate and NO(x) than Dahl salt-resistant rats on the same diet. It is known that urinary cyclic guanosine monophosphate and NO(x) represent the activity and stable derivatives of renal NO., respectively, and that they closely correlate with renal vascular resistance. Therefore, our results suggest that, in the Dahl salt-sensitive rat, increased oxidative stress is associated with salt-dependent hypertensive nephrosclerosis and that decreased NO. bioavailability may represent a common factor responsible for the vascular and glomerular dysfunction.
M R Trolliet; M A Rudd; J Loscalzo
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Kidney & blood pressure research     Volume:  24     ISSN:  1420-4096     ISO Abbreviation:  Kidney Blood Press. Res.     Publication Date:  2001  
Date Detail:
Created Date:  2001-07-03     Completed Date:  2001-10-25     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9610505     Medline TA:  Kidney Blood Press Res     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  116-23     Citation Subset:  IM    
Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, Boston, Mass 02118, USA.
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MeSH Terms
Cyclic GMP / metabolism
Diet, Sodium-Restricted
Dinoprost / analogs & derivatives,  metabolism
Dose-Response Relationship, Drug
Genetic Predisposition to Disease
Hypertension / chemically induced,  complications,  physiopathology*
Inulin / metabolism
Lipid Peroxidation
Metabolic Clearance Rate
Nephrosclerosis / etiology*,  metabolism
Nitrogen Oxides / metabolism
Oxidative Stress
Rats, Mutant Strains
Reactive Oxygen Species / metabolism*
Sodium Chloride, Dietary / toxicity*
Superoxides / metabolism
p-Aminohippuric Acid / metabolism
Grant Support
Reg. No./Substance:
0/F2-Isoprostanes; 0/Nitrogen Oxides; 0/Reactive Oxygen Species; 0/Sodium Chloride, Dietary; 11062-77-4/Superoxides; 27415-26-5/8-epi-prostaglandin F2alpha; 551-11-1/Dinoprost; 61-78-9/p-Aminohippuric Acid; 7665-99-8/Cyclic GMP; 9005-80-5/Inulin

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

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