Obesity induced renal oxidative stress contributes to renal injury in salt-sensitive hypertension

Jeffrey E. Quigley, Ahmed Abdelrazik Elmarakby, Sarah F. Knight, Marlina M. Manhiani, David W Stepp, Jeffrey J. Olearzcyk, John D. Imig

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

In the present study, we determined the role of hypertension, oxidative stress and inflammation on kidney damage in a rodent model of obesity and diabetes. Hypertension was induced in male obese (db/db) mice and lean (db/m) mice by implantation of deoxycorticosterone acetate (DOCA) pellets and mice were allowed to drink water containing 1% salt. Mice were divided into six groups as follows: obese and lean control, obese and lean 1% salt (salt) and obese and lean DOCA plus 1% salt (DOCA-salt). Blood pressure was significantly increased in lean and obese DOCA-salt groups relative to their respective controls; however, there was no difference in blood pressure between the lean and obese control and salt groups. Urinary 8-isoprostane was increased in obese control compared with lean control mice (1464 ± 267 vs 493 ± 53 pg/μmol creatinine, respectively) and this elevation was further increased in the obese DOCA-salt treated mice (2430 ± 312 pg/μmol creatinine). Urinary monocyte chemoattractant protein-1 excretion and CD68-positive cells were also increased in both obese and lean DOCA-salt groups compared with their respective controls. Furthermore, DOCA-salt treatment increased collagen IV excretion in both obese and lean mice compared with controls, but there was no difference between obese and lean DOCA-salt groups. Urinary albumin excretion was significantly increased in the obese compared with the lean DOCA-salt mice (507 ± 160 vs 202 ± 48 μg/day, respectively). These data suggest that obese DOCA-salt hypertensive mice exhibit greater renal injury than lean DOCA-salt hypertensive mice in a manner independent of blood pressure and that this renal injury is associated with obesity related pre-existing renal oxidative stress.

Original languageEnglish (US)
Pages (from-to)724-728
Number of pages5
JournalClinical and Experimental Pharmacology and Physiology
Volume36
Issue number7
DOIs
StatePublished - Jul 1 2009

Fingerprint

Desoxycorticosterone
Oxidative Stress
Obesity
Salts
Hypertension
Kidney
Acetates
Wounds and Injuries
8-epi-prostaglandin F2alpha
Blood Pressure
Creatinine
Obese Mice
Chemokine CCL2
Albumins
Rodentia
Collagen
Inflammation

Keywords

  • Db/db mice
  • Hypertension
  • Inflammation
  • Obesity
  • Oxidative stress

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Pharmacology

Cite this

Obesity induced renal oxidative stress contributes to renal injury in salt-sensitive hypertension. / Quigley, Jeffrey E.; Elmarakby, Ahmed Abdelrazik; Knight, Sarah F.; Manhiani, Marlina M.; Stepp, David W; Olearzcyk, Jeffrey J.; Imig, John D.

In: Clinical and Experimental Pharmacology and Physiology, Vol. 36, No. 7, 01.07.2009, p. 724-728.

Research output: Contribution to journalArticle

Quigley, Jeffrey E. ; Elmarakby, Ahmed Abdelrazik ; Knight, Sarah F. ; Manhiani, Marlina M. ; Stepp, David W ; Olearzcyk, Jeffrey J. ; Imig, John D. / Obesity induced renal oxidative stress contributes to renal injury in salt-sensitive hypertension. In: Clinical and Experimental Pharmacology and Physiology. 2009 ; Vol. 36, No. 7. pp. 724-728.
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AB - In the present study, we determined the role of hypertension, oxidative stress and inflammation on kidney damage in a rodent model of obesity and diabetes. Hypertension was induced in male obese (db/db) mice and lean (db/m) mice by implantation of deoxycorticosterone acetate (DOCA) pellets and mice were allowed to drink water containing 1% salt. Mice were divided into six groups as follows: obese and lean control, obese and lean 1% salt (salt) and obese and lean DOCA plus 1% salt (DOCA-salt). Blood pressure was significantly increased in lean and obese DOCA-salt groups relative to their respective controls; however, there was no difference in blood pressure between the lean and obese control and salt groups. Urinary 8-isoprostane was increased in obese control compared with lean control mice (1464 ± 267 vs 493 ± 53 pg/μmol creatinine, respectively) and this elevation was further increased in the obese DOCA-salt treated mice (2430 ± 312 pg/μmol creatinine). Urinary monocyte chemoattractant protein-1 excretion and CD68-positive cells were also increased in both obese and lean DOCA-salt groups compared with their respective controls. Furthermore, DOCA-salt treatment increased collagen IV excretion in both obese and lean mice compared with controls, but there was no difference between obese and lean DOCA-salt groups. Urinary albumin excretion was significantly increased in the obese compared with the lean DOCA-salt mice (507 ± 160 vs 202 ± 48 μg/day, respectively). These data suggest that obese DOCA-salt hypertensive mice exhibit greater renal injury than lean DOCA-salt hypertensive mice in a manner independent of blood pressure and that this renal injury is associated with obesity related pre-existing renal oxidative stress.

KW - Db/db mice

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KW - Inflammation

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