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Titolo:
Increased oxidative stress in experimental renovascular hypertension
Autore:
Lerman, LO; Nath, KA; Rodriguez-Porcel, M; Krier, JD; Schwartz, RS; Napoli, C; Romero, JC;
Indirizzi:
Mayo Clin & Mayo Fdn, Dept Internal Med, Div Hypertens, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 tens, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn, Dept Internal Med, Div Nephrol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 hrol, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn, Dept Internal Med, Div Cardiovasc Dis, Rochester, MN55905 USA Mayo Clin & Mayo Fdn Rochester MN USA 55905 c Dis, Rochester, MN55905 USA Mayo Clin & Mayo Fdn, Dept Physiol & Biophys, Rochester, MN 55905 USA MayoClin & Mayo Fdn Rochester MN USA 55905 phys, Rochester, MN 55905 USA Univ Naples, Dept Med, Naples, Italy Univ Naples Naples ItalyUniv Naples, Dept Med, Naples, Italy Univ Calif San Diego, Dept Med 0682, San Diego, CA 92103 USA Univ Calif San Diego San Diego CA USA 92103 0682, San Diego, CA 92103 USA
Titolo Testata:
HYPERTENSION
fascicolo: 2, volume: 37, anno: 2001,
parte:, 2 supplemento:, S
pagine: 541 - 546
SICI:
0194-911X(200102)37:2<541:IOSIER>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
RENAL-ARTERY STENOSIS; ANGIOTENSIN-II; IN-VIVO; RATS; KIDNEY; PLASMA; EXPRESSION; SUPEROXIDE; MECHANISM; INJURY;
Keywords:
hypertension, renal; angiotensin II; stress, oxidative; isoprostanes; renin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Lerman, LO Mayo Clin & Mayo Fdn, Dept Internal Med, Div Hypertens, 200 1stSt SW, Rochester, MN 55905 USA Mayo Clin & Mayo Fdn 200 1st St SW Rochester MN USA 55905 5 USA
Citazione:
L.O. Lerman et al., "Increased oxidative stress in experimental renovascular hypertension", HYPERTENSIO, 37(2), 2001, pp. 541-546

Abstract

The pathophysiological mechanisms responsible for maintenance of chronic renovascular hypertension remain undefined, Excess angiotensin II generationmay 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 sampleswere collected and renal blood flow measured with electron-beam computed tomography in pigs 5 and 10 weeks after induction of unilateral renal arterystenosis (n=7) or sham operation (n=7). Five weeks after procedure, plasmarenin activity and mean arterial pressure were elevated in hypertensive pigs. Levels of prostaglandin F2 alpha (PGF2 alpha)-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 reninactivity (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, PGF(2 alpha)-isoprostanes remain elevated, possiblydue 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.

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Documento generato il 01/12/20 alle ore 01:10:53