Oxidative stress contributes to sex differences in blood pressure in adult growth-restricted offspring

Norma B. Ojeda, Bettye Sue Hennington, Danielle T. Williamson, Melanie L. Hill, Nicole E E Betson, Julio Sartori Valinotti, Jane F. Reckelhoff, Thomas P. Royals, Barbara T. Alexander

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Numerous experimental studies suggest that oxidative stress contributes to the pathophysiology of hypertension and, importantly, that oxidative stress plays a more definitive role in mediating hypertension in males than in females. Intrauterine growth restriction induced by reduced uterine perfusion initiated at day 14 of gestation in the rat programs hypertension in adult male growth-restricted offspring; yet, female growth-restricted offspring are normotensive. The mechanisms mediating sex differences in blood pressure in adult growth-restricted offspring are not clear. Thus, this study tested the hypothesis that sex-specific differences in renal oxidative stress contribute to the regulation of blood pressure in adult growth-restricted offspring. A significant increase in blood pressure measured by telemetry in male growth-restricted offspring (P<0.05) was associated with a marked increase in renal markers of oxidative stress (P<0.05). Chronic treatment with the antioxidant Tempol had no effect on blood pressure in male control offspring, but it normalized blood pressure (P<0.05) and renal markers of oxidative stress (P<0.05) in male growth-restricted offspring relative to male control offspring. Renal markers of oxidative stress were not elevated in female growth-restricted offspring; however, renal activity of the antioxidant catalase was significantly elevated relative to female control offspring (P<0.05). Chronic treatment with Tempol did not significantly alter oxidative stress or blood pressure measured by telemetry in female offspring. Thus, these data suggest that sex differences in renal oxidative stress and antioxidant activity are present in adult growth-restricted offspring and that oxidative stress may play a more important role in modulating blood pressure in male but not female growth-restricted offspring.

Original languageEnglish (US)
Pages (from-to)114-122
Number of pages9
JournalHypertension
Volume60
Issue number1
DOIs
StatePublished - Jul 1 2012
Externally publishedYes

Fingerprint

Sex Characteristics
Oxidative Stress
Blood Pressure
Growth
Kidney
Telemetry
Antioxidants
Hypertension
Catalase
Perfusion
Pregnancy

Keywords

  • Antioxidant
  • Blood pressure
  • Intrauterine growth restriction

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Ojeda, N. B., Hennington, B. S., Williamson, D. T., Hill, M. L., Betson, N. E. E., Sartori Valinotti, J., ... Alexander, B. T. (2012). Oxidative stress contributes to sex differences in blood pressure in adult growth-restricted offspring. Hypertension, 60(1), 114-122. https://doi.org/10.1161/HYPERTENSIONAHA.112.192955

Oxidative stress contributes to sex differences in blood pressure in adult growth-restricted offspring. / Ojeda, Norma B.; Hennington, Bettye Sue; Williamson, Danielle T.; Hill, Melanie L.; Betson, Nicole E E; Sartori Valinotti, Julio; Reckelhoff, Jane F.; Royals, Thomas P.; Alexander, Barbara T.

In: Hypertension, Vol. 60, No. 1, 01.07.2012, p. 114-122.

Research output: Contribution to journalArticle

Ojeda, NB, Hennington, BS, Williamson, DT, Hill, ML, Betson, NEE, Sartori Valinotti, J, Reckelhoff, JF, Royals, TP & Alexander, BT 2012, 'Oxidative stress contributes to sex differences in blood pressure in adult growth-restricted offspring', Hypertension, vol. 60, no. 1, pp. 114-122. https://doi.org/10.1161/HYPERTENSIONAHA.112.192955
Ojeda, Norma B. ; Hennington, Bettye Sue ; Williamson, Danielle T. ; Hill, Melanie L. ; Betson, Nicole E E ; Sartori Valinotti, Julio ; Reckelhoff, Jane F. ; Royals, Thomas P. ; Alexander, Barbara T. / Oxidative stress contributes to sex differences in blood pressure in adult growth-restricted offspring. In: Hypertension. 2012 ; Vol. 60, No. 1. pp. 114-122.
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