Role of Oxidative Stress in Endothelial Dysfunction and Enhanced Responses to Angiotensin II of Afferent Arterioles from Rabbits Infused with Angiotensin II

Redox Control of Renal Function and Hypertension

“…Sufficient evidence supports the notion that Ang II promotes ROS formation via NAD(P)H oxidase activation by direct stimulatory effects (stimulation of the AT 1 R); studies on inhibition of the RAAS have contributed to this evidence as well (27,141,343,348,349,355). Renal afferent arterioles, when infused with Ang II at a slow pressor rate, exhibit renal cortical NAD(P)H-stimulated O 2 иϪ generation and lipid peroxidation in addition to impaired ACh-induced endothelium-dependent relaxation and enhanced contractile responses to Ang II.…”

“…Renal afferent arterioles, when infused with Ang II at a slow pressor rate, exhibit renal cortical NAD(P)H-stimulated O 2 иϪ generation and lipid peroxidation in addition to impaired ACh-induced endothelium-dependent relaxation and enhanced contractile responses to Ang II. The arterioles have a profound downregulation of the mRNA for AT 1 R but an upregulation of the p22 phox component of NAD(P)H oxidase (343). In addition, Ang II infusion in rats led to increased expression of NAD(P)H oxidase subunits, an effect abrogated with blockade of the AT 1 R. Moreover, administration of AT 2 R inhibitor PD-123,319 resulted in worsening of Ang II-mediated oxidative stress, as AT 2 R is known to mediate the beneficial effects of Ang II stimulation (27).…”

Haplotype analysis of NAD(P)H oxidase p22 phox polymorphisms in end-stage renal disease

“…The upregulation of NAD(P)H oxidase has been demonstrated in a chronic renal failure model (Vaziri et al 2003). NAD(P)H oxidase is also upregulated by angiotensin II in afferent arterioles of glomerulus (Wang et al 2003) and renal proximal tubular cells (Hannken et al 1998). The effects of angiotensin-converting enzyme (ACE) inhibitors have been demonstrated in both diabetic and nondiabetic renal diseases by large-scale clinical trials (Jafar et al 2001;Lewis et al 1993;Ruggenenti et al 1999) and ACE inhibitors are thought to have a renoprotective effect by ameliorating intraglomerular hypertension and reducing the degree of proteinuria as well as blood pressure.…”

A Water-Soluble Fullerene Vesicle Alleviates Angiotensin II-Induced Oxidative Stress in Human Umbilical Venous Endothelial Cells

“…Found initially in phagocytic cells, NAD(P)H oxidase has also been identified in non-phagocytic cells such as fibroblasts (2), endothelial cells (3), vascular smooth muscle cells (4), renal mesangial cells (5,6), and renal tubular cells (7,8). The upregulation of NAD(P)H oxidase by AII has been demonstrated in aortic vascular smooth muscle (9,10), afferent arterioles of the glomerulus (11), and endothelial cells. Reaction between the superoxide anion and nitric oxide will generate peroxynitrite, resulting in oxidative stresses that are highly damaging to endothelial cells.…”