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1 Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands
* To whom correspondence should be addressed. E-mail: G.B.Braam{at}azu.nl.
Wild-type mice are resistant to angiotensin II (Ang II)-induced renal injury and hence form an attractive model to study renal defense against Ang II. The present study tested whether Ang II induces expression of anti-oxidative genes via the AT2 receptor in renal cortex and thereby counteracts pro-oxidative forces. Ang II was infused in female C57Bl/6J mice for 28 days and a subgroup received AT2 receptor antagonist (PD-123,319) for the last three days. Ang II induced hypertension and aortic hypertrophy; proteinuria and renal injury were absent. Urinary NO metabolites (NOX) were decreased, lipid peroxide (TBARS) excretion remained unchanged. Expression of NADPH oxidase components was decreased in renal cortex, but induced in aorta. Heme oxygenase-1 (HO-1) was induced in both renal cortex and aorta. In contrast, Ang II suggestively increased AT2 receptor expression in kidney, but not in aorta. AT2 receptor blockade enhanced hypertension in Ang II-infused mice, reversed Ang II effects on NOX excretion, but did not affect TBARS. Despite its pro-hypertensive effect, expression of pro-oxidative genes in the renal cortex decreased rather than increased after short term AT2 receptor blockade and renal HO-1 induction after Ang II was normalized. Thus, chronic Ang II infusion in mice induces hypertension, but not oxidative stress. In contrast to the response in aorta, gene expression of components of NADPH-oxidase was not enhanced in renal cortex. Although Ang II administration induced renal cortical AT2 receptor expression, blockade of that receptor did not unveil the AT2 receptor as intrarenal dampening factor of pro-oxidative forces.
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