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Nitric Oxide Supplementation in Postischemic Acute Renal Failure: Normotension Versus Hypertension

Miloradović, Zoran; Mihailović-Stanojević, Nevena; Grujić-Milanović, Jelica; Ivanov, Milan; Jerkić, Mirjana; Jovović, Đurđica

(Bentham Science Publ Ltd, Sharjah, 2011)

TY  - JOUR
AU  - Miloradović, Zoran
AU  - Mihailović-Stanojević, Nevena
AU  - Grujić-Milanović, Jelica
AU  - Ivanov, Milan
AU  - Jerkić, Mirjana
AU  - Jovović, Đurđica
PY  - 2011
UR  - http://rimi.imi.bg.ac.rs/handle/123456789/373
AB  - Nitric oxide (NO) has been suggested to play a pivotal role in ischemic acute renal failure (ARF) but there are controversies about its role in hypertensive and non hypertensive ischemic kidney. Multiple strategies including administration of exogenous NO donors have been shown to protect the kidney against toxic or ischemic injury, suggesting endothelial dysfunction as impaired NO generation due to ischemia. However, in postischemic kidney, NO derived from inducible nitric oxide synthase (iNOS) has been considered to enhance the tissue damage while iNOS inhibition decreased the tubular damage. It is well known decrease in basal production of NO in essential hypertension and that long lasting hypertension damages medium size and small-size blood vessels, therefore predisposes nephroangiosclerosis patients to ARF. Many studies have shown that long term stimulation of NO release in normotension improves renal haemodymnamics and kidney function in ischemic form of ARF. On the other hand, there are studies that have shown that NO synthesis stimulation has no effect or even worsens tubular damage in postischemic hypertensive kidney. Therefore, it seems likely that NO supplementation plays different role in postischemic renal damage development, beneficial in well preserved normotensive kidney and limited in postischemic hypertensive kidney due to disturbed tubuloglomerular response, vasoreactivity and kidney vascular structure.
PB  - Bentham Science Publ Ltd, Sharjah
T2  - Current Pharmaceutical Biotechnology
T1  - Nitric Oxide Supplementation in Postischemic Acute Renal Failure: Normotension Versus Hypertension
EP  - 1367
IS  - 9
SP  - 1364
VL  - 12
DO  - 10.2174/138920111798281153
ER  - 
@article{
author = "Miloradović, Zoran and Mihailović-Stanojević, Nevena and Grujić-Milanović, Jelica and Ivanov, Milan and Jerkić, Mirjana and Jovović, Đurđica",
year = "2011",
abstract = "Nitric oxide (NO) has been suggested to play a pivotal role in ischemic acute renal failure (ARF) but there are controversies about its role in hypertensive and non hypertensive ischemic kidney. Multiple strategies including administration of exogenous NO donors have been shown to protect the kidney against toxic or ischemic injury, suggesting endothelial dysfunction as impaired NO generation due to ischemia. However, in postischemic kidney, NO derived from inducible nitric oxide synthase (iNOS) has been considered to enhance the tissue damage while iNOS inhibition decreased the tubular damage. It is well known decrease in basal production of NO in essential hypertension and that long lasting hypertension damages medium size and small-size blood vessels, therefore predisposes nephroangiosclerosis patients to ARF. Many studies have shown that long term stimulation of NO release in normotension improves renal haemodymnamics and kidney function in ischemic form of ARF. On the other hand, there are studies that have shown that NO synthesis stimulation has no effect or even worsens tubular damage in postischemic hypertensive kidney. Therefore, it seems likely that NO supplementation plays different role in postischemic renal damage development, beneficial in well preserved normotensive kidney and limited in postischemic hypertensive kidney due to disturbed tubuloglomerular response, vasoreactivity and kidney vascular structure.",
publisher = "Bentham Science Publ Ltd, Sharjah",
journal = "Current Pharmaceutical Biotechnology",
title = "Nitric Oxide Supplementation in Postischemic Acute Renal Failure: Normotension Versus Hypertension",
pages = "1367-1364",
number = "9",
volume = "12",
doi = "10.2174/138920111798281153"
}
Miloradović, Z., Mihailović-Stanojević, N., Grujić-Milanović, J., Ivanov, M., Jerkić, M.,& Jovović, Đ.. (2011). Nitric Oxide Supplementation in Postischemic Acute Renal Failure: Normotension Versus Hypertension. in Current Pharmaceutical Biotechnology
Bentham Science Publ Ltd, Sharjah., 12(9), 1364-1367.
https://doi.org/10.2174/138920111798281153
Miloradović Z, Mihailović-Stanojević N, Grujić-Milanović J, Ivanov M, Jerkić M, Jovović Đ. Nitric Oxide Supplementation in Postischemic Acute Renal Failure: Normotension Versus Hypertension. in Current Pharmaceutical Biotechnology. 2011;12(9):1364-1367.
doi:10.2174/138920111798281153 .
Miloradović, Zoran, Mihailović-Stanojević, Nevena, Grujić-Milanović, Jelica, Ivanov, Milan, Jerkić, Mirjana, Jovović, Đurđica, "Nitric Oxide Supplementation in Postischemic Acute Renal Failure: Normotension Versus Hypertension" in Current Pharmaceutical Biotechnology, 12, no. 9 (2011):1364-1367,
https://doi.org/10.2174/138920111798281153 . .
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