Increased Oxidative Stress in Experimental Renovascular Hypertension

摘要: The pathophysiological mechanisms responsible for maintenance of chronic renovascular hypertension remain undefined. Excess angiotensin II generation may lead to release reactive oxygen species and increased vasoconstrictor activity. To examine the potential involvement oxidation-sensitive in pathophysiology hypertension, blood samples were collected renal flow measured with electron-beam computed tomography pigs 5 10 weeks after induction unilateral artery stenosis (n=7) or sham operation (n=7). Five procedure, plasma renin activity mean arterial pressure elevated hypertensive pigs. Levels prostaglandin F2α (PGF 2α )–isoprostanes, vasoconstrictors markers oxidative stress, also significantly (157±21 versus 99±16 pg/mL; P r =0.83) ( =0.82). By weeks, returned baseline but remained (144±10 115±5 mm Hg; =0.7) not Stenotic kidney was decreased at both studies. In shock-frozen cortical tissue, ex vivo endogenous intracellular radical scavengers kidneys. present study demonstrates, first time, that early an increase is associated systemic stress. When later declines, PGF -isoprostanes elevated, possibly due local activation slow responses II, participate sustenance pressure. Moreover, influence ischemic parenchymal injury.