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Renal vasoconstrictor responses to norepinephrine and angiotensin II: Gender‐specific effects of extracellular superoxide dismutase deletion
Author(s) -
Wach Paul F,
Schneider Markus P,
Fukai Tohru,
Harrison David G,
Pollock David M,
Pollock Jennifer S
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1415-c
Subject(s) - norepinephrine , superoxide dismutase , angiotensin ii , endocrinology , extracellular , chemistry , medicine , renin–angiotensin system , superoxide , oxidative stress , receptor , biochemistry , enzyme , blood pressure , dopamine
Because of their ability to generate superoxide, we hypothesized that renal vasoconstrictor responses to norepinephrine (NE) and angiotensin II (Ang II) would be enhanced in mice lacking extracellular superoxide dismutase (ecSOD‐KO). NE (30 to 300 μg/kg) and Ang II (0.3 to 6 μg/kg) were administered (i.v.) to anesthetized male and female C57Bl/6 (WT) and ecSOD‐KO mice on a C57Bl/6 background (n=7–10). Blood pressure (BP) and renal blood flow (RBF) responses were measured via carotid artery catheter and ultrasonic flow probe, respectively. In WT mice, the decrease of RBF in response to NE was similar between males and females. RBF responses in male and female ecSOD‐KO mice to NE were reduced compared to male and female WT mice (e.g RBF response to 30 μg/kg NE in males: −7.9±1.2 vs −20.7±3.8%, p<0.0001; and in females: −12.2±2.3 vs −15.8±2.9%, p=0.04). However, responses in male ecSOD‐KO mice were attenuated to a greater extent than in female ecSOD‐KO mice, demonstrated by a lesser response in male versus females ecSOD‐KO mice (e.g RBF response to 30 μg/kg: −7.9±1.2 vs −12.2±2.3%, p=0.03). Similar results were found for BP responses to NE, and for RBF and BP responses to Ang II. Contrary to our hypothesis, renal vasoconstrictor responses in ecSOD‐KO mice were reduced. We hypothesize that male ecSOD‐KO mice have compensatory mechanisms that completely obviate the potential role of increased superoxide in the renal vasculature.