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CARDIAC, RENAL, AND RESPIRATORY INTEGRATION
Division of Nephrology and Hypertension and Center for Hypertension and Renal Disease Research, Georgetown University, Washington, District of Columbia 20007
Submitted 9 August 2002 ; accepted in final form 18 February 2003
Oxidative stress accompanies angiotensin (ANG) II infusion, but the role of ANG type 1 vs. type 2 receptors (AT1-R and AT2-R, respectively) is unknown. We infused ANG II subcutaneously in rats for 1 wk. Excretion of 8-isoprostaglandin F2
(8-Iso) and
malonyldialdehyde (MDA) were related to renal cortical mRNA abundance for
subunits of NADPH oxidase and superoxide dismutases (SODs) using real-time
PCR. Subsets of ANG II-infused rats were given the AT1-R antagonist
candesartan cilexetil (Cand) or the AT2-R antagonist PD-123,319
(PD). Compared to vehicle (Veh), ANG II increased 8-Iso excretion by 41% (Veh,
5.4 ± 0.8 vs. ANG II, 7.6 ± 0.5 pg/24 h; P < 0.05).
This was prevented by Cand (5.6 ± 0.5 pg/24 h; P < 0.05)
and increased by PD (15.8 ± 2.0 pg/24 h; P < 0.005). There
were similar changes in MDA excretion. Compared to Veh, ANG II significantly
(P < 0.005) increased the renal cortical mRNA expression of
p22phox (twofold), Nox-1 (2.6-fold), and Mn-SOD (1.5-fold)
and decreased expression of Nox-4 (2.1-fold) and extracellular (EC)-SOD
(2.1-fold). Cand prevented all of these changes except for the increase in
Mn-SOD. PD accentuated changes in p22phox and Nox-1 and
increased p67phox. We conclude that ANG II infusion
stimulates oxidative stress via AT1-R, which increases the renal
cortical mRNA expression of p22phox and Nox-1 and reduces
abundance of Nox-4 and EC-SOD. This is offset by strong protective effects of
AT2-R, which are accompanied by decreased expression of
p22phox, Nox-1, and p67phox.
candesartan; isoprostane; angiotensin receptor blocker; PD-123,319; malonyldialdehyde
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