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Articles in PresS, published online ahead of print May 6, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00602.2001
Submitted on October 3, 2001
Accepted on April 16, 2002
in normal and hypercholesterolemic pigs
1 Department of Internal Medicine, Division of Hypertension, Mayo Clinic, Rochester, MN, USA
2 Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, USA
3 Department of Physiology and Biophysics, Mayo Clinic, Rochester, MN, USA
* To whom correspondence should be addressed. E-mail: Lerman.Lilach{at}Mayo.Edu.
Hypercholesterolemia (HC) is characterized by increased circulating 8-epi-Prostaglandin-F2 (Isoprostane), vasoconstrictor, marker, and mediator of increased oxidative stress, whose vascular effects might be augmented in HC. Anesthetized pigs were studied in vivo with electron-beam computed-tomography after a 12-week normal (n=8) or HC (n=8) diet. Mean arterial pressure (MAP), single-kidney perfusion and glomerular filtration rate (GFR) were quantified before and during unilateral intra-renal infusions of U46619 (10 ng/kg/min) or Isoprostane (1µg/kg/min). Basal renal perfusion and function were similar, and Isoprostane infusion elevated its systemic levels similarly in normal and HC (333±89 vs. 366±48 pg/mL, respectively, p<0.01 vs. baseline). Both drugs markedly and comparably decreased cortical perfusion and GFR in both groups, while medullary perfusion decreased significantly only in HC. Moreover, MAP increased significantly only in HC (+9±3 and +11±3mmHg, respectively, p
0.05). Hence, in HC renal functional responses to high-dose Isoprostane are largely similar to normal, but the systemic circulation exhibits augmented sensitivity to pathophysiological levels of Isoprostane and U46619, which may potentially play a role in development of hypertension and vascular injury associated with increased oxidative-stress.
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