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Is there a relationship between the AT‐1 receptor and O2‐ in Renal Wrap Hypertension?
Author(s) -
Edwards Jennifer M,
Haywood Joseph R,
Northcott Carrie A
Publication year - 2006
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.20.4.a337-a
Subject(s) - endocrinology , medicine , nitrotyrosine , renal medulla , chemistry , nitric oxide , oxidative stress , kidney , superoxide dismutase , superoxide , receptor , mean arterial pressure , angiotensin ii , nitric oxide synthase , renin–angiotensin system , context (archaeology) , blood pressure , biology , heart rate , biochemistry , enzyme , paleontology
Angiotensin II (Ang II) has been implicated as a mediator of oxidative stress that contributes to hypertension via AT‐1 receptor activation and subsequent superoxide (O 2 ‐ ) production. We have previously shown plasma renin activity (PRA) to be increased at 7 days post‐wrap, but not elevated at 28 days. Furthermore, a dysregulation of nitric oxide synthase, nitrotyrosine, and superoxide dismutase expression in the kidney has been shown supporting the role of Ang II in this context. Thus, we hypothesized that there was an up‐regulation of AT‐1 receptor expression and O 2 − in the kidney in renal wrap hypertension. Rats were uninephrectomized and subjected to wrap/sham surgery and studied at 7 or 28 days. Kidneys from hypertensive wrap and normotensive sham rats were isolated; cortex and medulla were separated for protein isolation for western analysis or chemiluminescent O 2 − measurements (Mean Arterial Pressure; 7 day: Sham = 92 ± 4 mm Hg, Wrap = 139 ± 10 mm Hg; 28 day: Sham = 92 ± 6 mm Hg, Wrap =152 ± 7 mm Hg). At 7 days, there was a significant reduction in wrap medullary AT‐1 expression compared to sham (704 ± 252 vs. 2090 ± 476 arbitrary densitometry units), as well as medullary O 2 − production (10 ± 2 vs. 20 ± 4 pmol/min*mg). At 28 days, there were no changes in AT‐1 expression, but medullary O 2 − production was increased compared to sham (31 ± 3 vs. 19 ± 2 pmol/min*mg). No changes were found in cortical AT‐1 expression or O 2 − production at 7 or 28 days. The data suggest that during the onset of hypertension the elevated PRA may cause a down‐regulation of AT‐1 receptors and O 2 − in the renal medulla. During chronic hypertension, mechanisms other than Ang II are related to the increased O 2 − .