NADPH oxidase contributes to renal damage and dysfunction in Dahl salt-sensitive hypertension

Tian, Niu; Moore, Rebecca S.; Phillips, W. E. J.; Lin, Lin; Braddy, Sharkeshia J.; Pryor, Janelle S.; Stockstill, Rachel; Hughson, Michael D.; Manning, R. Davis

doi:10.1152/ajpregu.90650.2008

Cited by 64 publications

(56 citation statements)

References 49 publications

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“…The rise in arterial blood pressure in response to increased dietary salt intake in the MnSOD-deficient mice was accompanied by upregulation of NAD(P)H oxidase which is a major source of non-mitochondrial superoxide production in the renal and cardiovascular tissues. Upregulation of NAD(P)H oxidase in the kidney and vascular tissues is a common feature of nearly all models of acquired and hereditary hypertension [15][16][17][18]. Therefore, finding elevated renal tissue NAD(P)H oxidase in this model is consistent with that observed in other models of hypertension.…”

Section: Discussionsupporting

confidence: 87%

Salt-sensitive hypertension in mitochondrial superoxide dismutase deficiency is associated with intra-renal oxidative stress and inflammation

Jin

Vaziri

2013

Clin Exp Nephrol

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Section: Discussionsupporting

confidence: 87%

Salt-sensitive hypertension in mitochondrial superoxide dismutase deficiency is associated with intra-renal oxidative stress and inflammation

Jin

Vaziri

2013

Clin Exp Nephrol

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“…NADPH oxidase contributes importantly to renal cortical oxidative stress, inflammation, renal damage and dysfunction and increased in arterial pressure. 63 Previous study showed that the primary source of ROS generation in the renal cortex is NADPH oxidase. 64 NADPH oxidase is a cytoplasmic enzyme consisting of at least one catalytic, transmembrane-spanning NOX subunit, which produces ROS by transferring electrons from NADPH to molecular oxygen.…”

Section: 50mentioning

confidence: 99%

“…63 In conclusion, antioxidant NAC can confer protection against nitrosative and oxidative stresses in renal tissue induced by holoxan by suppressing renal NADPH oxidase activation, MDA, nitric oxide and restoring or enhancing SOD enzyme activity. Thus, inhibition of NADPH oxidase elevation level and activation led to subsequent reduction of ROS production and subsequently might effectively improve the gonadal hormone disturbance, sexual and reproductive functions.…”

mentioning

confidence: 91%

The effects ofN-acetyl-l-cysteine on the female reproductive performance and nephrotoxicity in rats

Helal

2016

Renal Failure

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This study was designed to investigate whether the treatment with the N-acetyl-L-cysteine prior to the administration of chemotherapy drug would prevent from nephrotoxicity and the loss of reproductive performance induced from chemotherapy treatment. Female rats were divided into five equal groups of six each: 1/control group; 2/rats i.p administered saline solution; 3/rats i.p administered holoxan (50 mg/kg b.wt); 4/rats i.p administered N-acetyl-L-cysteine (160 mg/kg b.wt); 5/rats i.p administered holoxan and N-acetyl-L-cysteine at the same doses. After medications, females rats were allowed to mate with males and the pregnant rats were sacrificed on day 18 of gestation. Premating treatment with holoxan showed reduction (p50.05) in reproductive performance. Whereas administration of N-acetyl-L-cysteine prior to treatment with holoxan and then concurrently with it modulated significantly fertility index, progesterone level, decreasing postimplantation loss, resorbed fetuses and improved fetal growth. Additionally, holoxan elevated the renal nicotinamide dinucleotide phosphate (NADPH) oxidase activity, oxidative stress, renal functions and caused histological changes in renal tissue. N-Acetyl-L-cysteine treatment reduced (p50.05) renal tissue NADPH oxidase, nitric oxide, malondialdehyde and improved super oxide dismutase (SOD) depletion, elevated levels phosphate, total protein and calcium as well as prevented renal histological damages. N-Acetyl-L-cysteine can confer protection against nitrosative and oxidative stresses in renal tissue induced by holoxan by suppressing NADPH oxidase activation, malondialdehyde, nitric oxide and restoring SOD activity which led to the reduction of reactive oxygen species production and subsequently might effectively improve the gonadal hormone disturbance and reproductive functions. ARTICLE HISTORY

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“…35 In the same rat model, an NADPH inhibitor, apocynin, also showed significant attenuation of proteinuria, as well as a significant reduction of SBP. 36 In this study, the significant reduction of p22 phox by combination therapy with irbesartan and efonidipine compared with irbesartan monotherapy may have contributed to the significant hypotensive effects seen with combination therapy compared with irbesartan alone.…”

Section: Discussionmentioning

confidence: 76%

Combination therapy with irbesartan and efonidipine for attenuation of proteinuria in Dahl salt-sensitive rats

2010

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Angiotensin receptor blockers (ARBs) or T-and L-type calcium channel blockers (CCBs) are useful for glomerular protection; however, the protective effects of combination therapy remain unclear. In this study, Dahl salt-sensitive rats were fed a high-salt diet and were treated daily with placebo, irbesartan (60 mg kg À1 ), efonidipine (30 mg kg À1 ), irbesartan (60 mg kg À1 )+efonidipine (30 mg kg À1 ), amlodipine (3 mg kg À1 ), or irbesartan (60 mg kg À1 )+amlodipine (3 mg kg À1 ) for 4 weeks. Significant reductions in systolic blood pressure were seen in the irbesartan-, efonidipine-and amlodipine-treated groups compared with the placebo-treated group; a further significant reduction was seen in the irbesartan+efonidipine-treated group compared with the irbesartan-treated group. Compared with the placebo-treated group, proteinuria was significantly lower in the irbesartan-and efonidipine-treated groups, but not in the amlodipine-treated group. Furthermore, a significant attenuation of proteinuria in the irbesartan+efonidipine-treated group compared with the irbesartan-treated group was observed; this effect was not observed in the irbesartan+amlodipine-treated group. The glomerulosclerosis index was significantly attenuated by all active treatments except amlodipine. The glomerulosclerosis index in the irbesartan+efonidipine-treated group, but not in the irbesartan+amlodipine-treated group, was significantly lower than that in the irbesartan-treated group. Significant attenuations of gene expressions of p22 phox , transforming growth factor-b, monocyte chemoattractant protein-1 and collegen I were observed in the irbesartan-and efonidipine-treated groups, but not in the amlodipine-treated group. Values for these parameters were reduced to control levels in the irbesartan+efonidipine-treated group. Combination therapy with ARB and T-and L-type CCB might produce a powerful renal protective effect. INTRODUCTIONKidneys have an important role not only in the homeostasis of water and electrolyte balance but also in the regulation of blood pressure. Angiotensin II is a crucial peptide for regulating blood pressure by slow and rapid pressor responses. The main functions of slow response are augmentation of sodium reabsorption in the proximal tubules and release of aldosterone from the adrenal cortex, whereas the main functions of rapid response are direct contractile response in peripheral resistance arteries and enhancement of peripheral noradrenergic neurotransmission. Therefore, blockade of angiotensin II is a useful antihypertensive strategy. In addition, angiotensin II directly increases mesangial matrix formation by stimulating transforming growth factor (TGF)-b expression. 1 Inhibition of angiotensin II function induces dilation of efferent arterioles, and this mechanism contributes to amelioration of glomerular hypertension, resulting in a decrease in mesangial matrix formation. 2 Therefore, blockade of angiotensin II is also useful for preventing glomerular injury.Calcium channel blockers (CCBs), such as angi...

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NADPH oxidase contributes to renal damage and dysfunction in Dahl salt-sensitive hypertension

Cited by 64 publications

References 49 publications

Salt-sensitive hypertension in mitochondrial superoxide dismutase deficiency is associated with intra-renal oxidative stress and inflammation

Salt-sensitive hypertension in mitochondrial superoxide dismutase deficiency is associated with intra-renal oxidative stress and inflammation

The effects ofN-acetyl-l-cysteine on the female reproductive performance and nephrotoxicity in rats

Combination therapy with irbesartan and efonidipine for attenuation of proteinuria in Dahl salt-sensitive rats

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