(Hypertension. 2001;37:541.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Increased Oxidative Stress in Experimental Renovascular Hypertension
From the Department of Internal Medicine, Divisions of Hypertension (L.O.L., J.D.K.), Nephrology (K.A.N.) and Cardiovascular Diseases (R.S.S.), and the Department of Physiology and Biophysics (J.C.R.), Mayo Clinic, Rochester, Minn; the Department of Medicine, University of Naples, Italy (C.N.); and the Department of Medicine-0682, University of California, San Diego, Calif (C.N.).
Correspondence to Lilach O. Lerman, MD, PhD, Division of Hypertension, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail lerman.lilach{at}mayo.edu
The
pathophysiological mechanisms responsible for
maintenance of chronic renovascular hypertension remain
undefined. Excess angiotensin II generation may lead to
release of reactive oxygen species and increased vasoconstrictor
activity. To examine the potential involvement of oxidation-sensitive
mechanisms in the pathophysiology of renovascular hypertension, blood
samples were collected and renal blood flow measured with electron-beam
computed tomography in pigs 5 and 10 weeks after induction of
unilateral renal artery stenosis (n=7) or sham operation (n=7).
Five weeks after procedure, plasma renin activity and mean
arterial pressure were elevated in hypertensive pigs.
Levels of prostaglandin F2
(PGF2)–isoprostanes, vasoconstrictors and
markers of oxidative stress, also were significantly increased (157±21
versus 99±16 pg/mL; P<0.05)
and correlated with both plasma renin activity
(r=0.83) and
arterial pressure
(r=0.82). By 10 weeks, plasma
renin activity returned to baseline but arterial pressure
remained elevated (144±10 versus 115±5 mm Hg;
P<0.05). Isoprostane levels
remained high and still correlated directly with the increase in
arterial pressure
(r=0.7) but not with plasma
renin activity. Stenotic kidney blood flow was decreased at
both studies. In shock-frozen cortical tissue, ex vivo
endogenous intracellular radical scavengers were
significantly decreased in both kidneys. The present study
demonstrates, for the first time, that in early renovascular
hypertension, an increase in plasma renin activity and
arterial pressure is associated with increased systemic
oxidative stress. When plasma renin activity later declines,
PGF2-isoprostanes remain elevated, possibly
due to local activation or slow responses to angiotensin
II, and may participate in sustenance of arterial pressure.
Moreover, oxidation-sensitive mechanisms may influence ischemic
and hypertensive parenchymal renal injury.
Key Words: hypertension, renal • angiotensin II • stress, oxidative • isoprostanes • renin
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