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Clinical Trial
. 1999 Aug;34(2):228-34.
doi: 10.1053/AJKD03400228.

Indices of activity of the nitric oxide system in hemodialysis patients

R J Schmidt  1 , J Domico, L S Samsell, S Yokota, T S Tracy, M I Sorkin, K Engels, C Baylis
Affiliations
Clinical Trial

Indices of activity of the nitric oxide system in hemodialysis patients

R J Schmidt et al. Am J Kidney Dis. 1999 Aug.

Abstract

Arginine deficiency and/or increased levels of circulating nitric oxide (NO) synthesis (NOS) inhibitors can cause reduced NOS, which may contribute to hypertension in patients with end-stage renal disease (ESRD). To test these hypotheses, NO oxidation products (NO(2) + NO(3) = NO(x)) and cyclic guanosine monophosphate (cGMP), the vasodilatory second messenger of NO, were measured in the blood, urine, and dialysate effluent of hemodialysis (HD) patients and compared with the blood and urine of healthy subjects. The subjects ate a controlled low-nitrate diet (approximately 330 micromol/d) for 48 hours before and during blood, dialysis effluent, and 24-hour urine collection. NO(x) output was significantly reduced in HD patients versus controls (552 +/- 51 v 824 +/- 96 micromol/24 h; P < 0.001), whereas cGMP output was not low versus controls. Plasma arginine level was normal and plasma levels of citrulline and the endogenous NOS inhibitor, asymmetric dimethylarginine (ADMA), were markedly elevated in patients with ESRD versus controls. Systolic blood pressure was greater in HD patients compared with controls despite concurrent antihypertensive therapy in most patients with ESRD. These studies suggest NO production is low in patients with ESRD undergoing HD, possibly because of the increased ratio of plasma ADMA to arginine.

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Figures

Fig 1
Fig 1. Standard curves for lNMA, ADMA, and SDMA, which are linear in the concentration range of 0.625 to 10.0 μmol/L
Fig 2
Fig 2. Representative chromatograms for (top) control plasma, (middle) HD patient plasma, and (bottom) control plasma spiked with 2.5 μmol/L of lNMA, ADMA, and SDMA. All peaks are within the linear range of the standard curves shown in Fig 1
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References

    1. Kone BC, Baylis C. Biosynthesis and homeostatic roles of nitric oxide in the kidney. Editorial review. Am J Physiol. 1997;272:F561–F578. - PubMed
    1. Moncada S, Palmer RMJ, Higgs EA. Nitric oxide: Physiology, pathophysiology, and pharmacology. Pharmacol Rev. 1991;43:109–141. - PubMed
    1. Baylis C, Vallance P. Nitric oxide and BP: Effects of NO deficiency. Curr Opin Nephrol Hypertens. 1996;5:80–88. - PubMed
    1. Mailloux LU, Haley WE. Hypertension in the ESRD patient: Pathophysiology, therapy, outcomes and future directions. Am J Kidney Dis. 1998;32:705–719. - PubMed
    1. United States Renal Data System. USRDS 1990 Annual Data Report. The National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; Bethesda, MD: 1990.

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