Role of nitric oxide synthase activity in experimental ischemic acute renal failure in rats.
To determine the role of nitric oxide (NO) in acute renal failure (ARF), we have studied the time course change activities to activity of nitric oxide synthase (NOS) isoform activities, both calcium dependent and independent NOS, in experimental ischemic ARF. We have also analyzed change activities to activity of the NOS activities in both renal cortex and medulla. Male SD rats (n = 5) were inducted to ARF by ischemia-reperfusion injury and divided into the following groups; Control group (sham operation), Day 0 group, (measurement performed on that day of operation), Day 1 group, (measurement performed one day after induction of ARF), Day 3 group and Day 7 group. Measurement of NOS activity was based on the following principles; NO is synthesized from arginine by nitric oxide synthase (NOS) and NO is converted to NO2(-)/NO3(-)(NOx) by oxidation. Detection of the final metabolite of NO, NOx was done using flow injection method (Griess reaction). The results were, (1) calcium dependent NOS activity in the cortex and medulla decreased, however it increased in the recovery period in the renal cortex (Cortex; Control, 0.941 +/- 0.765, D0, 0.382 +/- 0.271, D1, 0.118 +/- 0.353, D3, 2.030 +/- 0.235, D7, 3.588 +/- 2.706, Medulla; Control, 1.469 +/- 0.531, D0, 0.766 +/- 0.156, D1, 0.828 +/- 0.187, D3, 2.078 +/- 0.094, D7, 1.289 +/- 0.313 micromol NOx produced/mg protein/30 min). (2) On the other hand, iNOS activity increased in the early phase of ARF, both in the cortex and medulla, but returned to control values during the recovery phase in cortex and was maintained at higher levels in the medulla (Cortex; Control, 0.333 +/- 0.250, D0, 0.583 +/- 0.428, D1, 1.167 +/- 0.262, D3, 0.250 +/- 0.077, D7, 0.452 +/- 0.292, Medulla; Control, 0.139 +/- 0.169, D0, 0.279 +/- 0.070, D1, 1.140 +/- 0.226, D3, 0.452 +/- 0.048, D7, 0.625 +/- 0.048 micromol NOx produced/mg protein/30 min). These findings suggest that the role of NOS in ARF are different for the different NOS isoforms and have anatomic heterogeneity.
Komurai
Mild
M
St. Marianna University School of Medicine, Department of Internal Medicine, Division of Nephrology and Hypertension, Kawasaki, Japan.
Ishii
Yasuko
Y
Matsuoka
Fumiaki
F
Toyama
Katsuhide
K
Ominato
Masayuki
M
Sato
Takeo
T
Maeba
Teruhiko
T
Kimura
Kenjiro
K
Owada
Shigeru
S
D058186:Acute Kidney Injury / Q000201:enzymology* / Q000378:metabolism; D000818:Animals; D001835:Body Weight; D002118:Calcium / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D007668:Kidney / Q000378:metabolism; D008297:Male; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000502:physiology*; D020033:Protein Isoforms; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury; D013997:Time Factors
D020033:Protein Isoforms; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D002118:Calcium