EFFECT OF INHIBITION OF NEURONAL NITRIC OXIDE SYNTHASE AND <scp>l</scp>‐ARGININE SUPPLEMENTATION ON RENAL ISCHAEMIA–REPERFUSION INJURY AND THE RENAL NITRIC OXIDE SYSTEM

Rusai, Krisztina; Fekete, Andrea; Szebeni, Beáta; Vannay, Ádám; Bokodi, Géza; Müller, Veronika; Viklický, Ondřej; Bloudíčková, Silvie Rajnochová; Rajnoch, J; Heemann, Uwe; Reusz, György; Szabó, András; Tulassay, Tivadar; Szabó, Attila

doi:10.1111/j.1440-1681.2008.04976.x

Cited by 14 publications

(12 citation statements)

References 41 publications

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“…35 Ischemia decreases L-ARG concentrations in the renal cortex and medulla, resulting in a decreased substrate supply for NO synthesis. This situation can be reversed by exogenous supplementation of L-ARG, 38 as was also demonstrated in this study.…”

Section: Discussionsupporting

confidence: 60%

“…35 We found that exogenous administration of L-ARG for 21 days increased the expression of eNOS, nNOS and iNOS. Rusai et al 38 showed that, in kidneys that underwent ischemia, supplementation with L-ARG for 7 days increased the expression of mRNA for the three isoforms of NOS. Intrarenal NO production stimulated by L-ARG also increases renal sodium excretion by a direct tubular action and by regulating vascular tone in the pressure natriuretic response in the renal medulla.…”

Section: Discussionmentioning

confidence: 98%

“…33 Thus, nNOS protein levels have been reported to correlate inversely with developing kidney damage. 38 In the renal cortex, nNOS mediates the synthesis of renin, dilates the afferent arterioles and reduces the reabsorption of sodium. 32 Our data demonstrate a decrease in the expression of nNOS in the non-clipped kidney of 2K1C rats, which is directly related to the pathophysiology of the hypertensive model, demonstrating hemodynamic changes in both kidneys.…”

Section: Discussionmentioning

confidence: 99%

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Combined Aliskiren and L-arginine treatment reverses renovascular hypertension in an animal model

et al. 2015

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Renovascular hypertension is characterized by increased renal sympathetic activity, angiotensin II and by endothelial dysfunction. The purpose of this study was to determine the role of renal sympathetic nerve activity (RSNA) in mediating the anti-hypertensive effects of aliskiren (ALSK) and L-arginine (L-ARG) in a rat renovascular hypertension model. Hypertension was induced by clipping the right renal artery, and the following five groups were divided: SHAM operated; 2-kidney, 1-clip (2K1C); 2K1C plus ALSK; 2K1C plus L-ARG; and 2K1C plus ALSK+ L-ARG. The systolic blood pressure (SBP) of 2K1C rats increased from 114.4±5.2 to 204±12.7 mm Hg (P<0.05) and was only reduced by ALSK+L-ARG treatment (138.4±4.37 mm Hg). The 2K1C hypertension increased the baseline RSNA (SHAM: 62.4±6.39 vs. 2K1C: 97.4±8.43%). L-ARG or ALSK+L-ARG treatment significantly decreased baseline RSNA (2K1C L-ARG:70.7±2.39; 2K1C ALSK+L-ARG: 69.3±4.23%), but ALSK treatment alone did not (2K1C ALSK: 84.2±2.5%). Urinary water, Na(+), Cl(-) and urea excretion were similar in the 2K1C L-ARG, 2K1C ALSK+L-ARG and SHAM groups. The combination of ALSK+L-ARG restored urine flow and increased the glomerular filtration rate. The nNOS expression in the non clipped kidney was significantly increased in 2K1C ALSK+L-ARG rats. In conclusion, combined ALSK+L-ARG treatment normalizes SBP and prevents renal dysfunction in 2K1C hypertensive rats.

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Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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Combined Aliskiren and L-arginine treatment reverses renovascular hypertension in an animal model

et al. 2015

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“…However, a more recent study by Rusai et al in the ischemic rat kidney, observed that L-arginine (2 g/kg body weight daily) didn't affect the injury sustained from I/R, but did increase the mRNA expression of NOS isoforms. This may be explained by time and dose administration differences between studies, along with the severity of the ischemic injury [90]. Again, more studies examining the ideal dose and time of administration of L-arginine will be helpful in determining its possible therapeutic value.…”

Section: Endogenous No: L-argininementioning

confidence: 95%

Nitric Oxide Mechanism of Protection in Ischemia and Reperfusion Injury

Phillips

Toledo

López-Neblina

et al. 2009

Journal of Investigative Surgery

174

107

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In 1992 nitric oxide (NO) was declared molecule of the year by Science magazine, and ever since research on this molecule continues to increase. Following this award, NO was shown to be a mediator/protector of ischemia and reperfusion injury in many organs, such as the heart, liver, lungs, and kidneys. Controversy has existed concerning the actual protective effects of NO. However, literature from the past 15 years seems to reinforce the consensus that NO is indeed protective. Some of the protective actions of NO in ischemia and reperfusion are due to its potential as an antioxidant and anti-inflammatory agent, along with its beneficial effects on cell signaling and inhibition of nuclear proteins, such as NF-kappa B and AP-1. New therapeutic potentials for this drug are also continuously emerging. Exogenous NO and endogenous NO may both play protective roles during ischemia and reperfusion injury. Sodium nitroprusside and nitroglycerin have been used clinically with much success; though only recently have they been tested and proven effective in attenuating some of the injuries associated with ischemia and reperfusion. NO inhalation has, in the past, mostly been used for its pulmonary effects, but has also recently been shown to be protective in other organs. The potential of NO in the treatment of ischemic disease is only just being realized. Elucidation of the mechanism by which NO exerts its protective effects needs further investigation. Therefore, this paper will focus on the mechanistic actions of NO in ischemia and reperfusion injury, along with the compound's potential therapeutic benefits.

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“…Data regarding the impact of L-Arg on the regulation of the expression of genes and proteins for all NOS isoforms are scarce. Rusai et al have demonstrated that L-Arg supplementation for seven days in rats with a model of renal ischemia increased the mRNA expression of all three NOS isoforms, but increased only NOS II protein levels [40].…”

Section: Discussionmentioning

confidence: 99%

Renal Response to L-Arginine in Diabetic Rats. A Possible Link between Nitric Oxide System and Aquaporin-2

et al. 2014

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The aim of this study was to evaluate whether L-Arginine (L-Arg) supplementation modifies nitric oxide (NO) system and consequently aquaporin-2 (AQP2) expression in the renal outer medulla of streptozotocin-diabetic rats at an early time point after induction of diabetes. Male Wistar rats were divided in four groups: Control, Diabetic, Diabetic treated with L-Arginine and Control treated with L-Arginine. Nitric oxide synthase (NOS) activity was estimated by [14C] L-citrulline production in homogenates of the renal outer medulla and by NADPH-diaphorase staining in renal outer medullary tubules. Western blot was used to detect the expression of AQP2 and NOS types I and III; real time PCR was used to quantify AQP2 mRNA. The expression of both NOS isoforms, NOS I and NOS III, was decreased in the renal outer medulla of diabetic rats and L-Arg failed to prevent these decreases. However, L-Arg improved NO production, NADPH-diaphorase activity in collecting ducts and other tubular structures, and NOS activity in renal homogenates from diabetic rats. AQP2 protein and mRNA were decreased in the renal outer medulla of diabetic rats and L-Arg administration prevented these decreases. These results suggest that the decreased NOS activity in collecting ducts of the renal outer medulla may cause, at least in part, the decreased expression of AQP2 in this model of diabetes and constitute additional evidence supporting a role for NO in contributing to renal water reabsorption through the modulation of AQP2 expression in this pathological condition. However, we cannot discard that another pathway different from NOS also exists that links L-Arg to AQP2 expression.

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EFFECT OF INHIBITION OF NEURONAL NITRIC OXIDE SYNTHASE AND l‐ARGININE SUPPLEMENTATION ON RENAL ISCHAEMIA–REPERFUSION INJURY AND THE RENAL NITRIC OXIDE SYSTEM

Cited by 14 publications

References 41 publications

Combined Aliskiren and L-arginine treatment reverses renovascular hypertension in an animal model

Combined Aliskiren and L-arginine treatment reverses renovascular hypertension in an animal model

Nitric Oxide Mechanism of Protection in Ischemia and Reperfusion Injury

Renal Response to L-Arginine in Diabetic Rats. A Possible Link between Nitric Oxide System and Aquaporin-2

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