To test the hypothesis that nitric oxide (NO) deficiency occurs in end-stag
e renal disease (ESRD), NO oxidation products (NO2 + NO3 = NOx) and cGMP we
re measured in blood, urine, and dialysate effluent of peritoneal dialysis
(PD) patients and compared with blood and urine of healthy subjects. All su
bjects were on a controlled low-nitrate diet (similar to 330 mu mol/day). N
Ox and cGMP outputs were significantly reduced in PD patients (334 +/- 50 m
u mol/24 h and 55 +/- 13 nmol/24 h, respectively) vs. controls (823 +/- 101
mu mol/24 h and 149 +/- 46 nmol/24 h). Plasma arginine was borderline low,
plasma citrulline was elevated and plasma levels of the endogenous NO synt
hase inhibitor asymmetric dimethylarginine were approximately five time hig
her in PD patients (2.2 +/- 0.3 mu M) vs. controls (0.4 +/- 0.1 mu M). Alth
ough blood pressure (BP) was not different between groups at the time of st
udy, 10 of 11 PD patients were on medication for hypertension. These studie
s demonstrate that total NO production is low in ESRD, and with appropriate
caution, we conclude that this NO deficiency may contribute to the increas
ed BP that occurs in ESRD.