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Am J Physiol Renal Physiol 276: F794-F797, 1999;
0363-6127/99 $5.00
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Vol. 276, Issue 5, F794-F797, May 1999

RAPID COMMUNICATION
Nitric oxide production is low in end-stage renal disease patients on peritoneal dialysis

Rebecca J. Schmidt1, Stanley Yokota2, Timothy S. Tracy3, Michael I. Sorkin1, and Chris Baylis2

1 Departments of Medicine, 3 Basic Pharmaceutical Sciences, and 2 Physiology, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, West Virginia 26506

To test the hypothesis that nitric oxide (NO) deficiency occurs in end-stage renal disease (ESRD), NO oxidation products (NO2 + NO3 = NOx) and cGMP were measured in blood, urine, and dialysate effluent of peritoneal dialysis (PD) patients and compared with blood and urine of healthy subjects. All subjects were on a controlled low-nitrate diet (~330 µmol/day). NOx and cGMP outputs were significantly reduced in PD patients (334 ± 50 µmol/24 h and 55 ± 13 nmol/24 h, respectively) vs. controls (823 ± 101 µmol/24 h and 149 ± 46 nmol/24 h). Plasma arginine was borderline low, plasma citrulline was elevated and plasma levels of the endogenous NO synthase inhibitor asymmetric dimethylarginine were approximately five time higher in PD patients (2.2 ± 0.3 µM) vs. controls (0.4 ± 0.1 µM). Although blood pressure (BP) was not different between groups at the time of study, 10 of 11 PD patients were on medication for hypertension. These studies demonstrate that total NO production is low in ESRD, and with appropriate caution, we conclude that this NO deficiency may contribute to the increased BP that occurs in ESRD.

hypertension; arginine; citrulline; guanosine 3',5'-cyclic monophosphate; endogenous nitric oxide synthase inhibitors


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