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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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