Effect of nitric oxide synthesis modification on renal function in gentamicin-induced nephrotoxicity

Valdivielso, José M.; Rivas-Cabañero, Lina; Pérez‐Barriocanal, Fernando; López‐Novoa, José M.

doi:10.1016/s1382-6689(97)00148-8

Cited by 11 publications

(5 citation statements)

References 34 publications

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“…All these data suggest a protective role for NO in the bilateral renal ischemia. Something similar has been reported for gentamicin-induced renal failure (25). A further proof of the beneficial role of NO in ischemic renal failure is the fact that the administration of exogenous NO donors had been shown to be unequivocally beneficial against ischemia-induced renal failure and tubular necrosis (4,10).…”

Section: Discussionsupporting

confidence: 60%

“…These conclusions come from the lack of response to NO-dependent vasodilators as a result of ischemic endothelial injury (6,13). Recently, several papers have suggested that NO is involved in the maintenance of RBF, urinary flow, and GFR in rats with ARF (5,8,25). Noiri et al (18) reported an increased inducible NOS (iNOS)-derived NO production in ischemic kidneys and that inhibition of iNOS expression decreased the tubular damage.…”

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confidence: 99%

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Renal ischemia in the rat stimulates glomerular nitric oxide synthesis

Valdivielso¹,

Crespo²,

Alonso³

et al. 2001

American Journal of Physiology-Regulatory, Integrative and Comp

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Renal ischemia in humans and in experimental animals is associated with a complex and possibly interrelated series of events. In this study, we have investigated the glomerular nitric oxide (NO) production after renal ischemia. Unilateral or bilateral renal ischemia was induced in Wistar rats by clamping one or both renal arteries. NO production was assessed by measuring glomerular production of nitrite, a stable end product of NO catabolism, and NO-dependent glomerular cGMP production and by assessing the glomerular NADPH diaphorase (ND) activity, an enzymatic activity that colocalizes with NO-synthesis activity. Furthermore, we determined the isoform of NO synthase (NOS) implicated in NO synthesis by Western blot and immunohistochemistry. Glomeruli from rats with bilateral ischemia showed elevated glomerular nitrite and cGMP production. Besides, glomeruli from this group of rats showed an increased ND activity, whereas glomeruli from the ischemic and nonischemic rats with unilateral ischemia did not show this increase in nitrite, cGMP, and ND activity. In addition, glomeruli from ischemic kidneys showed an increased expression of endothelial NOS without changes in the inducible isoform. Addition of L-NAME in the drinking water induced a higher increase in the severity of the functional and structural damage in rats with bilateral ischemia than in rats with unilateral ischemia and in sham-operated animals. We can conclude that after renal ischemia, there is an increased glomerular NO synthesis subsequent to an activation of endothelial NOS that plays a protective role in the renal damage induced by ischemia and reperfusion.

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Section: Discussionsupporting

confidence: 60%

mentioning

confidence: 99%

Renal ischemia in the rat stimulates glomerular nitric oxide synthesis

Valdivielso¹,

Crespo²,

Alonso³

et al. 2001

American Journal of Physiology-Regulatory, Integrative and Comp

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“…, 2003). Valdivielso et al (1997) demonstrated that chronic stimulation of nitric oxide (NO) synthesis partially prevented gentamicin‐nephrotoxicity, thus suggesting that increased renal NO synthesis may play a protective role on renal function during gentamicin‐induced‐nephrotoxicity. Abdel‐Naim et al.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, of diallyl disulfide which is a garlic-derived compound with antioxidant properties has been evaluated for its possible renoprotective effects in gentamicin-induced nephrotoxicity in rats (Pedraza-Chaverrı et al, 2003). Valdivielso et al (1997) demonstrated that chronic stimulation of nitric oxide (NO) synthesis partially prevented gentamicin-nephrotoxicity, thus suggesting that increased renal NO synthesis may play a protective role on renal function during gentamicin-inducednephrotoxicity. Abdel-Naim et al (1999) and Kumar et al (2000) noted that the antioxidant activity of vitamin E and probucol had potentially protective effects against gentamicininduced nephrotoxicity and observed that co-administration of these agents had produced a more pronounced improvement in urine gamma-glutamyl transferase and N-acetyl-b D-glucosaminidase and serum creatinine and urea concentrations.…”

Section: Discussionmentioning

confidence: 99%

Effect of silymarin and vitamin E on gentamicin‐induced nephrotoxicity in dogs

Varzi

Esmailzadeh

Morovvati

et al. 2007

Vet Pharm & Therapeutics

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Drug-induced nephrotoxicity is an important cause of renal failure in dogs. Aminoglycoside antibiotics, such as gentamicin, can produce nephrotoxicity in dogs, due to in part to an imbalance of pro- and antioxidants (oxidative stress). Silymarin (the mixture of flavonolignans extracted from Silybum marianum) has potentially beneficial antioxidant properties. A control group (saline, group 1, n = 5) was compared with dogs that were administrated gentamicin by intramuscular injection, at dosage of 20 mg/kg, once daily for 9 days (groups 2-5, n = 5 per group). The effects of vitamin E (group 3) and silymarin (group 4) alone and in combination (group 5) were compared for induced nephrotoxicity. Renal function was assessed using serum biochemical markers (creatinine and urea). Malondialdehyde (MDA) concentration were measured as a marker of lipid peroxidation. The activity of total serum antioxidants (TSAO) was assessed as a marker of antioxidant defences. Serum creatinine and urea concentrations were increased significantly and TSAO was decreased significantly in group 2 compared with group 1. Serum creatinine concentrations but not urea concentrations were significantly lower in groups 3 and 4 than in group 2 (P = 0.001). Serum MDA concentrations was significantly different between groups 2 and 3 (P = 0.01), 2 and 4 (P < 0.001) and 4 and 5 (P = 0.01). TSAO activity was significantly in group 4 (silymarin) than in group 2 (P = 0.002). Silymarin and vitamin E decreased gentamicin-induced nephrotoxicity in dogs.

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“…Rectal temperature was monitored with a thermometer and maintained at 37.5 ЊC. Animals were surgical prepared and clearance of [metoxy-14 C]inulin and [ 3 H]para-aminohippuric acid (PAH) were made to estimate GFR and renal plasma flow (RPF) as previously described (Valdivielso et al 1997).…”

Section: Renal Function Studiesmentioning

confidence: 99%

Increased renal glomerular endothelin‐1 release in gentamicin‐induced nephrotoxicity

Valdivielso

Rivas-Cabañero²,

Morales³

et al. 1999

Int J Experimental Path

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Gentamicin-induced acute renal failure is characterized by a decrease in renal plasma flow and creatinine clearance. Endothelins (ET) are potent renal vasoconstrictors. The aim of this work is to assess the role of ET-1 in gentamicin-induced renal failure. Renal glomerular release of ET-1 was measured in rats with gentamicin-induced nephrotoxicity (100 mg/kg/day, s.c. for 2, 4 or 6 days). Glomeruli were isolated and incubated for 24 h in RPMI-1640. Glomerular supernatant and plasma concentration of ET-1 were measured by RIA. Renal failure was assessed by insulin, para-aminohippuric and creatinine clearance and histological studies. Gentamicin induced a dose number-dependent increase in plasma creatinine and a decrease in creatinine clearance. This was accompanied by a marked decrease in inulin and para-aminohippuric acid clearance, as well as by a marked tubular necrosis, without alterations in glomerular structures. Plasma ET-1 concentration and glomerular ET-1 release were also increased in gentamicin-treated rats. When 10-5 M gentamicin was added to control glomeruli, ET-1 production was not modified (36.4 +/- 2.2 vs. 35.2 +/- 1.7 pg/ml/24 h). All these results suggest that elevated ET-1 plasma levels and increased glomerular release of ET-1 could mediate, at least in part, the decrease in glomerular filtration rate observed in gentamicin-induced ARF.

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Effect of nitric oxide synthesis modification on renal function in gentamicin-induced nephrotoxicity

Cited by 11 publications

References 34 publications

Renal ischemia in the rat stimulates glomerular nitric oxide synthesis

Renal ischemia in the rat stimulates glomerular nitric oxide synthesis

Effect of silymarin and vitamin E on gentamicin‐induced nephrotoxicity in dogs

Increased renal glomerular endothelin‐1 release in gentamicin‐induced nephrotoxicity

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