Nitric Oxide Supplementation in Postischemic Acute Renal Failure: Normotension Versus Hypertension
Нема приказа
Аутори
Miloradović, ZoranMihailović-Stanojević, Nevena
Grujić-Milanović, Jelica
Ivanov, Milan
Jerkić, Mirjana
Jovović, Đurđica
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
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.
Кључне речи:
Acute renal failure / hypertension / kidney / nitric oxideИзвор:
Current Pharmaceutical Biotechnology, 2011, 12, 9, 1364-1367Издавач:
- Bentham Science Publ Ltd, Sharjah
Финансирање / пројекти:
- Улога биолошки активних молекула у експерименталним моделима кардиоваскуларних обољења (RS-145054)
- [SK-SRB-0026-09]
DOI: 10.2174/138920111798281153
ISSN: 1389-2010
PubMed: 21554222
WoS: 000294896500009
Scopus: 2-s2.0-80052257390
Институција/група
Institut za medicinska istraživanjaTY - 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 . .