(Hypertension. 1999;34:983-986.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Low-Dose Angiotensin II Increases Free Isoprostane Levels in Plasma
From the Department of Physiology and Biophysics, Mayo School of Medicine and Mayo Clinic, Rochester, Minn.
Abstract—Chronic
intravenous infusion of subpressor doses of
angiotensin II causes blood pressure to increase
progressively over the course of several days. The mechanisms
underlying this response, however, are poorly understood. Because
high-dose angiotensin II increases oxidative stress, and
some compounds that result from the increased oxidative stress (eg,
isoprostanes) produce vasoconstriction and antinatriuresis, we tested
the hypothesis that a subpressor dose of angiotensin II
also increases oxidative stress, as measured by
8-epi-prostaglandin F2
(isoprostanes), which
may contribute to the slow pressor response to angiotensin
II. To test this hypothesis, we infused angiotensin II (10
ng/kg per minute for 28 days via an osmotic pump) into 6 conscious
normotensive female pigs (30 to 35 kg). We recorded mean
arterial pressure continuously with a telemetry system and
measured plasma isoprostanes before starting the
angiotensin II infusion (baseline) and again after 28 days
with an enzyme immunoassay. Angiotensin II infusion
significantly increased mean arterial pressure from 121±4
to 153±7 mm Hg (P<0.05) without altering total
plasma isoprostane levels (180.0±24.3 versus 147.0±29.2 pg/mL;
P=NS). However, the plasma concentrations of free
isoprostanes increased significantly, from 38.3±5.8 to 54.7±10.4
pg/mL (P<0.05). These results suggest that subpressor
doses of angiotensin II increase oxidative stress, as
implied by the increased concentration of free isoprostanes, which
accompany the elevation in mean arterial pressure
elevation. Thus, isoprostane-induced vasoconstriction and
antinatriuresis may contribute to the hypertension induced by the slow
pressor responses of angiotensin II.
Key Words: kidney • oxidative stress • prostaglandins • lipid peroxidation
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