Decreased excretion of nitrate and nitrite in essential hypertensives with renal vasoconstriction

Sierra, Milagros; González, Álvaro; Gómez-Alamillo, C.; Monreal, Ignacío; Huarte, Emma; Gil, Ana Gloria; Sánchez-Casajús, Ángel; Díez, Javier

doi:10.1038/sj.ki.4490557

Cited by 6 publications

(3 citation statements)

References 22 publications

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“…Since the excretion of serum nitrite and nitrate is via renal route [21], it is unlikely that the elevated serum NO metabolites found in BA patients were secondary to liver impairment. One of the problems is that we do not know which organs are responsible for the elevated NO production in BA patients.…”

Section: Discussionmentioning

confidence: 98%

Elevated serum nitric oxide metabolites in biliary atresia

et al. 2005

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Biliary atresia (BA) remains one of the most intractable liver diseases in children. The aim of this study was to investigate the possible roles of nitric oxide (NO) in BA. Serum levels of nitrite and nitrate (NO production) were determined using a colorimetric method from 65 post-operative BA patients and 12 healthy children. The patients were categorized into two groups according to their jaundice status, and serum alanine aminotransferase (ALT, a marker for liver injury). Unpaired t tests were used. Data are expressed as mean and SD in terms of mumol/l. Age and gender between BA patients and controls were comparable. Serum NO metabolites of BA patients was higher than the controls (79.77+/-21.22 vs. 65.75+/-9.44, P=0.001). Subgroup analysis revealed that there was no difference in serum nitrate/nitrite levels of BA patients without jaundice compared to those with jaundice (78.85+/-23.23 vs. 80.90+/-18.76, P=0.70). However, patients with serum ALT> or =100 IU/l had higher levels of serum NO metabolites compared to those with serum ALT<100 IU/l. In conclusion, NO production was elevated in BA patients compared to normal controls. Serum NO was associated with serum ALT levels, but not with jaundice status, in BA patients. These suggest that NO plays a role in the pathophysiology of liver injury in post-operative BA.

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Section: Discussionmentioning

confidence: 98%

Elevated serum nitric oxide metabolites in biliary atresia

et al. 2005

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“…The final products of NO in vivo are NO 2 - and NO 3 - . Therefore, urinary excretion of NO 2 - plus NO 3 - is determined as an index of NO production, and the levels of products of the arginine-NO pathway, such as NO 2 - and NO 3 - , in biological fluids can be used as clinical markers for monitoring certain pathologic conditions and the progress of their treatment ( , ). Noris et al () reported that arginine levels and NO synthesis are higher in uremics than healthy volunteers, suggesting an explanation for the increased NO synthesis in uremia.…”

Section: Discussionmentioning

confidence: 99%

Influence of Green Tea Polyphenol in Rats with Arginine-Induced Renal Failure

Yokozawa¹,

Cho²,

Nakagawa³

2003

J. Agric. Food Chem.

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To determine whether green tea polyphenol ameliorates the pathological conditions induced by excessive dietary arginine, green tea polyphenol was administered to rats at a daily dose of 50 or 100 mg/kg body weight for 30 days with a 2% w/w arginine diet. In arginine-fed control rats, urinary and/or serum levels of guanidino compounds, nitric oxide (NO), urea, protein, and glucose increased significantly, while the renal activities of the oxygen species-scavenging enzymes superoxide dismutase (SOD) and catalase decreased, compared with casein-fed rats. However, rats given green tea polyphenol showed significant and dose-dependent decreases in serum levels of creatinine (Cr) and urea nitrogen and urinary excretion of Cr, and they exerted a slight reduction of nitrite plus nitrate, indicating that green tea polyphenol reduced the production of uremic toxins and NO. In addition, in arginine-fed rats the urinary urea, protein, and glucose level increases were reversed by the administration of green tea polyphenol. Moreover, in rats given green tea polyphenol the SOD and catalase activities suppressed by excessive arginine administration increased dose-dependently, implying the biological defense system was augmented as a result of free radical scavenging. These results suggest that green tea polyphenol would ameliorate renal failure induced by excessive dietary arginine by decreasing uremic toxin, and NO production and increasing radical-scavenging enzyme activity.

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“…Since activation of ET B receptors leads to a variety of intracellular events, of which NO release is the major one, nonfunctional ET B receptors or reduced ET-1 levels in the renal tissue should be associated with diminished excretion of NO metabolites (NO 2 + NO 3 ) in the urine of hypertensive patients. Indeed, Sierra et al (13) demonstrated that urinary excretion of NO 2 + NO 3 was lower in most hypertensive patients, especially those with high renal vascular resistance, than in normotensive subjects. Since NO plays an important role in the regulation of medullary blood flow (1), impairment of NO production may reduce intrarenal blood flow and subsequently reset the pressurenatriuresis relationship, leading to prompt sodium retention and contributing to high blood pressure.…”

Section: Renal Et and Hypertensionmentioning

confidence: 99%

The Intrarenal Endothelin System and Hypertension

et al. 2001

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The kidney is both a source of endothelin (ET) generation and an important target organ of this peptide. The highest concentrations of ET-1 in the body exist in the renal medulla, where it mediates natriuretic and diuretic effects through the ET(B) receptor subtype. It is proposed that aberrations in the renal ET system may lead to sodium and water retention and subsequently to the development of hypertension.

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Decreased excretion of nitrate and nitrite in essential hypertensives with renal vasoconstriction

Cited by 6 publications

References 22 publications

Elevated serum nitric oxide metabolites in biliary atresia

Elevated serum nitric oxide metabolites in biliary atresia

Influence of Green Tea Polyphenol in Rats with Arginine-Induced Renal Failure

The Intrarenal Endothelin System and Hypertension

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