Long-term antioxidant administration attenuates mineralocorticoid hypertension and renal inflammatory response

Richard A. Beswick, Hanfang Zhang, Dawnyetta Marable, John D. Catravas, William D Hill, R Clinton Webb

Research output: Contribution to journalArticle

192 Citations (Scopus)

Abstract

We previously reported increased monocyte/macrophage infiltration, reactive oxygen species accumulation, and nuclear factor-κB (NF-κB) activation in mineralocorticoid (deoxycorticosterone acetate [DOCA]) hypertensive rats. We tested the hypothesis that prolonged antioxidant administration inhibits superoxide accumulation, lowers blood pressure, and reduces NF-κB activation in DOCA-salt hypertensive rats. DOCA rats exhibited a significant increase in systolic blood pressure compared with sham rats. Aortic rings from DOCA rats exhibited increased superoxide (O 2 - ) production compared with sham rats. In addition, the treatment of DOCA rats with pyrrolidinedithiocarbamate (PDTC) or 4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl (Tempol) caused a significant decrease in systolic blood pressure and aortic superoxide accumulation. Monocyte/macrophage infiltration was also significantly decreased in DOCA rats treated with PDTC or Tempol compared with untreated DOCA rats. NF-κB-binding activity was significantly greater in untreated DOCA rats than in either sham rats or PDTC- or Tempol-treated DOCA rats. Also, DOCA rats treated with Tempol exhibited no significant difference in NF-κB-binding activity compared with sham. These results suggest that antioxidants attenuate systolic blood pressure, suppress renal NF-κB-binding activity, and partly alleviate renal monocyte/macrophage infiltration in DOCA-salt hypertension.

Original languageEnglish (US)
Pages (from-to)781-786
Number of pages6
JournalHypertension
Volume37
Issue number2 II
StatePublished - Mar 19 2001

Fingerprint

Mineralocorticoids
Renal Hypertension
Desoxycorticosterone
Antioxidants
Acetates
Blood Pressure
Superoxides
Monocytes
Macrophages
Salts
Kidney
Reactive Oxygen Species

Keywords

  • Hypertension
  • Mineralocorticoid
  • Monocyte/macrophage
  • Nuclear factor-κB
  • Pyrrolidinedithiocarbamate
  • Tempol

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Beswick, R. A., Zhang, H., Marable, D., Catravas, J. D., Hill, W. D., & Webb, R. C. (2001). Long-term antioxidant administration attenuates mineralocorticoid hypertension and renal inflammatory response. Hypertension, 37(2 II), 781-786.

Long-term antioxidant administration attenuates mineralocorticoid hypertension and renal inflammatory response. / Beswick, Richard A.; Zhang, Hanfang; Marable, Dawnyetta; Catravas, John D.; Hill, William D; Webb, R Clinton.

In: Hypertension, Vol. 37, No. 2 II, 19.03.2001, p. 781-786.

Research output: Contribution to journalArticle

Beswick, RA, Zhang, H, Marable, D, Catravas, JD, Hill, WD & Webb, RC 2001, 'Long-term antioxidant administration attenuates mineralocorticoid hypertension and renal inflammatory response', Hypertension, vol. 37, no. 2 II, pp. 781-786.
Beswick, Richard A. ; Zhang, Hanfang ; Marable, Dawnyetta ; Catravas, John D. ; Hill, William D ; Webb, R Clinton. / Long-term antioxidant administration attenuates mineralocorticoid hypertension and renal inflammatory response. In: Hypertension. 2001 ; Vol. 37, No. 2 II. pp. 781-786.
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