Nitric Oxide and Acute Renal Failure

Nephron ◽  
1996 ◽  
Vol 73 (3) ◽  
pp. 375-381 ◽  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Acute Renal Failure

Nitric oxide in ischaemic acute renal failure of streptozotocin diabetic rats

Diabetologia ◽  
1996 ◽  
Vol 39 (9) ◽  
pp. 1036-1040 ◽  
Author(s):  
Y. Goor ◽  
G. Peer ◽  
A. Iaina ◽  
M. Blum ◽  
Y. Wollman ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Diabetic Rats ◽  
Streptozotocin Diabetic Rats

Nitric oxide(NO) in the pathogenesis of acute renal failure (ARF) in rats

1995 ◽  
Vol 31 ◽  
pp. 354
Author(s):  
F.U. Dzgoeva ◽  
Yu.U. Milovanov ◽  
O.V. Zozulya ◽  
I.M. Kutyrina
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Acute Renal Failure

scholarly journals ROLE OF NITRIC OXIDE IN POSTISCHEMIC EXPERIMENTAL ACUTE RENAL FAILURE

1997 ◽  
Vol 75 ◽  
pp. 83
Author(s):  
M Jerkić ◽  
J Varagić ◽  
D Jovović ◽  
D Nastić-Mirić ◽  
G Adanja-Grujić ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Acute Renal Failure

Impaired tubulointerstitial expression of endothelin-1 and nitric oxide isoforms in donor kidney biopsies with postischemic acute renal failure

2003 ◽  
Vol 76 (4) ◽  
pp. 715-720 ◽  
Author(s):  
Christa Mitterbauer ◽  
Christoph Schwarz ◽  
Peter Hauser ◽  
Rudolf Steininger ◽  
Heinz M. Regele ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Donor Kidney ◽  
Endothelin 1

Endothelial nitric oxide synthase-deficient mice exhibit increased susceptibility to endotoxin-induced acute renal failure

2004 ◽  
Vol 287 (5) ◽  
pp. F1044-F1048 ◽  
Author(s):  
Wei Wang ◽  
Amit Mitra ◽  
Brian Poole ◽  
Sandor Falk ◽  
M. Scott Lucia ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Knockout Mice ◽  
Endothelial Nitric Oxide Synthase ◽  
Wild Type ◽  
In The Wild ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Acute renal failure (ARF) in septic patients drastically increases the mortality to 50–80%. Nitric oxide (NO) has been shown to be increased in sepsis. Endothelial nitric oxide synthase (eNOS) is one of the major regulators of arterial blood pressure and regional blood flow; however, its in vivo role in septic ARF is still unclear. We hypothesized that eNOS affords a protective effect against the renal vasoconstriction during endotoxemia. Because there are no specific inhibitors for eNOS, the study was therefore undertaken in eNOS knockout mice. There was no significant difference in baseline glomerular filtration rate (GFR) between the wild-type mice and the eNOS knockout mice (140 ± 10 vs. 157 ± 18 μl/min, n = 9, P = not significant). However, renal blood flow (RBF) was significantly decreased in eNOS knockout mice compared with the wild-type controls (0.62 ± 0.05 ml/min, n = 6 vs. 0.98 ± 0.13 ml/min, n = 8, P < 0.05). Mean arterial pressure (MAP) was significantly higher in eNOS knockout mice than the wild-type controls (109 ± 5 vs. 80 ± 1 mmHg, n = 10, P < 0.01). Thus renal vascular resistance (RVR) was much higher in eNOS knockout mice than in the wild-type mice (176 ± 2, n = 6 vs. 82 ± 1 mmHg·ml−1·min−1, n = 8, P < 0.01). When 1.0 mg/kg LPS was injected, there was no change in MAP in either the wild-type (84 ± 3 mmHg, n = 10) or the eNOS knockout mice (105 ± 5 mmHg, n = 10). Although GFR (154 ± 22 μl/min, n = 8) and RBF (1.19 ± 0.05 ml/min, n = 9) remained unchanged with the 1.0-mg/kg dose of LPS in the wild-type mice, GFR (83 ± 18 vs. 140 ± 10 μl/min, n = 6, P < 0.01) and RBF (0.36 ± 0.04 vs. 0.62 ± 0.05 ml/min, n = 6, P < 0.01) decreased significantly in the eNOS knockout mice. Fractional excretion of sodium increased significantly in eNOS knockout mice during endotoxemia (3.61 ± 0.78, n = 7 vs. 0.95 ± 0.14, n = 6, P < 0.01), whereas it remained unchanged in the wild-type mice (0.59 ± 0.16, n = 9 vs. 0.42 ± 0.05, n = 6, P = not significant). In summary, eNOS knockout mice have increased RVR and are more susceptible to endotoxemic ARF than wild-type mice despite higher MAP.

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