Document Detail

Exercise reduces oxidative stress but does not alleviate hyperinsulinemia or renal dopamine D1 receptor dysfunction in obese rats.
MedLine Citation:
PMID:  20926629     Owner:  NLM     Status:  MEDLINE    
Impairment of renal dopamine D1 receptor (D1R)-mediated natriuresis is associated with hypertension in humans and animal models, including obese Zucker rats. We have previously reported that treatment of these rats with antioxidants or insulin sensitizers reduced insulin levels and oxidative stress, restored D1R-mediated natriuresis, and reduced blood pressure. Furthermore, the redox-sensitive transcription factor, nuclear factor-κB (NF-κB), has been implicated in impairment of D1R-mediated natriuresis during oxidative stress. In this study, we investigated the effect of exercise on insulin levels, oxidative stress, nuclear translocation of NF-κB, blood pressure, albuminuria, and D1R-mediated natriuresis. The exercise protocol involved treadmill exercise from 3 wk of age for 8 wk. Exercise reduced oxidative stress, nuclear translocation of NF-κB, and albuminuria. However, exercise did not reduce plasma insulin levels or blood pressure. Also, selective D1R agonist (SKF-38393)-mediated increases in sodium excretion and guanosine 5'-O-(3-thiotriphosphate) binding were impaired in obese rats compared with lean rats, and exercise did not restore this defect. We conclude that, while exercise is beneficial in reducing oxidative stress and renal injury, reducing insulin levels may be required to restore D1R-mediated natriuresis in this model of obesity and metabolic syndrome. Furthermore, this study supports previous observations that restoring D1R function contributes to blood pressure reduction in this model.
Abdul Bari Muhammad; Mustafa F Lokhandwala; Anees A Banday
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Publication Detail:
Type:  Journal Article     Date:  2010-10-06
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  300     ISSN:  1522-1466     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-07     Completed Date:  2011-02-09     Revised Date:  2011-04-28    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F98-104     Citation Subset:  IM    
Heart and Kidney Institute, College of Pharmacy, S & R-2 Bldg, University of Houston, 4800 Calhoun Rd., Houston, TX 77204, USA.
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MeSH Terms
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / pharmacology
Albuminuria / prevention & control
Hyperinsulinism / prevention & control*
Insulin / blood
NF-kappa B / metabolism
Oxidative Stress
Physical Conditioning, Animal / physiology*
Protein Transport / drug effects
Rats, Zucker
Receptors, Dopamine D1 / agonists,  physiology*
Reg. No./Substance:
0/NF-kappa B; 0/Receptors, Dopamine D1; 11061-68-0/Insulin; 67287-49-4/2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine

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

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