Dietary L-Arginine Supplementation Improves the Glomerular Filtration Rate and Renal Blood Flow After 24 Hours of Unilateral Ureteral Obstruction in Rats

Ito, Keiichi; Chen, Jie; Vaughan, E. Darracott; Seshan, Surya V.; Poppas, Dix P.; Felsen, Diane

doi:10.1097/01.ju.0000105073.67242.eb

Cited by 29 publications

(34 citation statements)

References 17 publications

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“…apoptotic cells when HKC-8 cells were subjected to pressure of 60 mmHg for 18 h (Fig. 2C) (6,18,29). The earliest increase in iNOS expression was documented at 10 min following UUO (15).…”

Section: Resultsmentioning

confidence: 99%

“…Increasing NO metabolites has been shown to be protective in UUO (18). The irreversible inhibitor 1400W significantly increased HKC-8 cell death at 30 and 60 min [3 Ϯ 0.01 vs. 12 Ϯ 0.03% (P Ͻ 0.05, 30 min), 9 Ϯ 0.01 vs. 16 Ϯ 0.01% (P Ͻ 0.05, 60 min); Fig.…”

Section: Effect Of Nf-b Inhibition On Inos Expressionmentioning

confidence: 99%

“…It has been reported that exogenous nitrates, L-arginine or iNOS gene transfection, restored renal blood flow (RBF), glomerular filtration rates (GFR) and reduced renal injury (15,17,18). Recently, Ito et al (18) and Valles et al (43) reported increased iNOS expression in animal models of UUO and unilateral ureteropelvic junction obstruction (UPJ) in children, respectively. In addition, Hegarty et al (15) documented an early increase in iNOS protein expression, at 10 min following UUO.…”

mentioning

confidence: 96%

“…Several studies showed that NO has a restorative effect on renal function and injury in obstructed kidneys (6,15,18). It has been reported that exogenous nitrates, L-arginine or iNOS gene transfection, restored renal blood flow (RBF), glomerular filtration rates (GFR) and reduced renal injury (15,17,18).…”

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confidence: 99%

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Early upregulation of iNOS mRNA expression and increase in NO metabolites in pressurized renal epithelial cells

Broadbelt¹,

Stahl²,

Chen³

et al. 2007

American Journal of Physiology-Renal Physiology

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“…apoptotic cells when HKC-8 cells were subjected to pressure of 60 mmHg for 18 h (Fig. 2C) (6,18,29). The earliest increase in iNOS expression was documented at 10 min following UUO (15).…”

Section: Resultsmentioning

confidence: 99%

Section: Effect Of Nf-b Inhibition On Inos Expressionmentioning

confidence: 99%

mentioning

confidence: 96%

mentioning

confidence: 99%

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Early upregulation of iNOS mRNA expression and increase in NO metabolites in pressurized renal epithelial cells

Broadbelt¹,

Stahl²,

Chen³

et al. 2007

American Journal of Physiology-Renal Physiology

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“…Reduced levels of L-arginine have been observed in renal failure, but the clinical relevance is uncertain, as the measured serum concentrations are well in excess of the K m for eNOS (1,38). Nevertheless, both clinical (20,47,52,60) and experimental studies (12,14,18,22,23,36,44) have demonstrated that substrate supplementation stimulates NO production and attenuates renal damage and salt-sensitive hypertension. Furthermore, chronic NO inhibition with N G -nitro-Larginine methyl ester (L-NAME), an antagonist for L-arginine, causes salt-sensitive hypertension and the development of renal injury (62).…”

mentioning

confidence: 99%

Role of nitric oxide deficiency in the development of hypertension in hydronephrotic animals

Carlström¹,

Brown²,

Edlund³

et al. 2008

American Journal of Physiology-Renal Physiology

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Role of nitric oxide deficiency in the development of hypertension in hydronephrotic animals. Am J Physiol Renal Physiol 294: F362-F370, 2008. First published November 21, 2007 doi:10.1152/ajprenal.00410.2007.-Hydronephrotic animals develop renal injury and hypertension, which is associated with an abnormal tubuloglomerular feedback (TGF). The TGF sensitivity is coupled to nitric oxide (NO) in the macula densa. The involvement of reduced NO availability in the development of hypertension in hydronephrosis was investigated. Hydronephrosis was induced by ureteral obstruction in young rats. Blood pressure and renal excretion were measured in adulthood, under different sodium conditions, and before and after chronic administration of either N G -nitro-L-arginine methyl ester (L-NAME) or L-arginine. Blood samples for ADMA, SDMA, and L-arginine analysis were taken and the renal tissue was used for histology and determination of NO synthase (NOS) proteins. TGF characteristics were determined by stop-flow pressure technique before and after administration of 7-nitroindazole (7-NI) or L-arginine. Hydronephrotic animals developed salt-sensitive hypertension, which was associated with pressure natriuresis and diuresis. The blood pressure response to L-NAME was attenuated and L-arginine supplementation decreased blood pressure in hydronephrotic animals, but not in the controls. Under control conditions, reactivity and sensitivity of the TGF response were greater in the hydronephrotic group. 7-NI administration increased TGF reactivity and sensitivity in control animals, whereas, in hydronephrotic animals, neuronal NOS (nNOS) inhibition had no effect. L-Arginine attenuated TGF response more in hydronephrotic kidneys than in controls. The hydronephrotic animals displayed various degrees of histopathological changes. ADMA and SDMA levels were higher and the renal expressions of nNOS and endothelial NOS proteins were lower in animals with hydronephrosis. Reduced NO availability in the diseased kidney in hydronephrosis, and subsequent resetting of the TGF mechanism, plays an important role in the development of hypertension.ADMA; tubuloglomerular feedback; L-arginine; L-NAME; telemetry; blood pressure HYPERTENSION IS THE MOST COMMON chronic disorders worldwide and secondary forms of hypertension are found in 5-10% of the hypertensive population, of which most can be linked to renal disease (24). In humans, as well as in experimental models of salt-sensitive hypertension, there is a growing body of evidence pointing at a close relationship between nitric oxide (NO) deficiency and development of hypertension (37).Hydronephrosis due to obstruction at the level of the pelvicureteric junction is a common condition in children, with an incidence in newborns of ϳ1%. The obstruction is mostly partial and congenital of origin. Unilateral hydronephrosis causes salt-sensitive hypertension in both rats (5) and mice (7).The renal function in hydronephrotic animals, measured as renal blood flow and glomerular filtration rate (GFR), is rather...

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Photoacoustic Imaging of Nanoparticle Transport in the Kidneys at High Temporal Resolution

Jiang

Tang

et al. 2019

Angewandte Chemie

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Dietary L-Arginine Supplementation Improves the Glomerular Filtration Rate and Renal Blood Flow After 24 Hours of Unilateral Ureteral Obstruction in Rats

Abstract: This study demonstrates that L-arginine supplementation can improve renal function in acute UUO. This finding suggests that NO system may be a future site of pharmacological intervention for UUO.

Cited by 29 publications

References 17 publications

Early upregulation of iNOS mRNA expression and increase in NO metabolites in pressurized renal epithelial cells

Early upregulation of iNOS mRNA expression and increase in NO metabolites in pressurized renal epithelial cells

Role of nitric oxide deficiency in the development of hypertension in hydronephrotic animals

Photoacoustic Imaging of Nanoparticle Transport in the Kidneys at High Temporal Resolution

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