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. 2010 Sep;56(3):325-30.
doi: 10.1161/HYPERTENSIONAHA.109.142422. Epub 2010 Jul 19.

Reactive oxygen species, NADPH oxidases, and hypertension

Srinivasa Raju Datla  1 , Kathy K Griendling
Affiliations

Reactive oxygen species, NADPH oxidases, and hypertension

Srinivasa Raju Datla et al. Hypertension. 2010 Sep.
No abstract available

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Figures

Figure 1
Figure 1. Neuronal NADPH oxidase-dependent ROS involved in central regulation of hypertension
NADPH oxidase homologues, mainly Nox2 and Nox4, are found in different regions of the neuronal system and are reported to have a role in the neuropathogenesis of hypertension by enhancing the sympathetic nerve activity. Nox-induced ROS initiate a forward loop (1) in cross activation of different receptors and (2) between Nox and mitochondrial ROS. SFO, subfornical organ; OVLT, organum vasculosum of the lamina terminalis; PVN, paraventricular nucleus; PP, posterior pituitary; AP, area postrema; NTS, nucleus tractus solitarius; RVLM, rostral ventrolateral medulla.
Figure 2
Figure 2. Renal NADPH oxidase-dependent ROS involved in functional alterations of the kidney in hypertension
NADPH oxidase homologues, mainly Nox2 and Nox4, are expressed in different regions of the renal system and regulate normal kidney function and end organ damage in hypertension. Similar to neuronal ROS, Nox-induced ROS initiate a forward loop in (1) cross activation of different receptors in podocytes and (2) cross-talk between organ systems like central ROS-induced renal inflammation. THAL, thick ascending limb of the loop of Henle.
Figure 3
Figure 3. Vascular NADPH oxidase-dependent ROS and vascular function
NADPH oxidases play an important role in normal vascular signaling and vascular dysfunction. Endothelial and vascular smooth muscle Nox-derived ROS inactivate NO and initiate a forward loop (1) in cross activation of different receptors (orange arrows), (2) between ROS sources (blue arrows), and (3) in cross-talk between organ systems like central ROS induced vascular inflammation (red arrows). AT1R, Angiotensin type 1 receptors; MR, mineralocorticoid receptors; Nox, NADPH oxidases; MC, mitochondria; NOS, nitric oxide synthase; NO, nitric oxide; ONOO-, peroxynitrite; EC, endothelial cells; VSMC, Vascular smooth muscle cells; Trx, thioredoxin 2; MitoQ10, mitochondrial-targeted antioxidant; SOD3, superoxide dismutase-3; Gpx-1, glutathione peroxidase-1.
See this image and copyright information in PMC

References

    1. Sun C, Sellers KW, Sumners C, Raizada MK. NAD(P)H Oxidase Inhibition Attenuates Neuronal Chronotropic Actions of Angiotensin II. Circ Res. 2005;96:659–666. - PubMed
    1. Ye S, Zhong H, Campese VM. Oxidative Stress Mediates the Stimulation of Sympathetic Nerve Activity in the Phenol Renal Injury Model of Hypertension. Hypertension. 2006;48:309–315. - PubMed
    1. Fujita M, Ando K, Nagae A, Fujita T. Sympathoexcitation by Oxidative Stress in the Brain Mediates Arterial Pressure Elevation in Salt-Sensitive Hypertension. Hypertension. 2007;50:360–367. - PubMed
    1. Lob HE, Marvar PJ, Guzik TJ, Sharma S, McCann LA, Weyand C, Gordon FJ, Harrison DG. Induction of Hypertension and Peripheral Inflammation by Reduction of Extracellular Superoxide Dismutase in the Central Nervous System. Hypertension. 2010;55:277–283. - PMC - PubMed
    1. Peterson JR, Burmeister MA, Tian X, Zhou Y, Guruju MR, Stupinski JA, Sharma RV, Davisson RL. Genetic Silencing of Nox2 and Nox4 Reveals Differential Roles of These NADPH Oxidase Homologues in the Vasopressor and Dipsogenic Effects of Brain Angiotensin II. Hypertension. 2009;54:1106–1114. - PMC - PubMed