The role of renal sympathetic nervous system in the pathogenesis of ischemic acute renal failure

Fujii, Toshihide; Kurata, Hayato; Takaoka, Masanori; Muraoka, Tomoko; Fujisawa, Yoshihide; Shokoji, Takatomi; Nishiyama, Akira; Abe, Youichi; Matsumura, Yasuo

doi:10.1016/j.ejphar.2003.09.036

Cited by 105 publications

(112 citation statements)

References 17 publications

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“…15,16) We also found that ischemia/reperfusion-induced ARF was attenuated by a surgical or pharmacological blockade of renal sympathetic nerve, followed by a suppression of elevated renal venous norepinephrine levels. 17) Similar suppressive effect on renal venous norepinephrine levels were also observed in rats given i.v. bolus injection of L-carnosine (1-10 mg/kg).…”

Section: Discussionsupporting

confidence: 64%

Retraction：Dietary Supplementation of L-Carnosine Prevents Ischemia/Reperfusion-Induced Renal Injury in Rats

Fujii

Takaoka

Tsuruoka

et al. 2005

Biological & Pharmaceutical Bulletin

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Section: Discussionsupporting

confidence: 64%

Retraction：Dietary Supplementation of L-Carnosine Prevents Ischemia/Reperfusion-Induced Renal Injury in Rats

Fujii

Takaoka

Tsuruoka

et al. 2005

Biological & Pharmaceutical Bulletin

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“…Indeed, increased renal sympathetic nerve activity during and after ischemic AKI increases renal vein catecholamines released to systemic circulation and directly contributes to increased renal injury after IR. 33 Furthermore, a previous study by Jiang et al showed that renal denervation increased plasma and kidney renalase levels. 34 Therefore, renal sympathetic nerve activation may negatively modulate kidney and plasma renalase levels.…”

Section: Discussionmentioning

confidence: 99%

Renalase Protects against Ischemic AKI

Lee¹,

Kim²,

Kim³

et al. 2013

Journal of the American Society of Nephrology

120

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Elevated levels of plasma catecholamines accompany ischemic AKI, possibly contributing the inflammatory response. Renalase, an amine oxidase secreted by the proximal tubule, degrades circulating catecholamines and reduces myocardial necrosis, suggesting that it may protect against renal ischemia reperfusion injury. Here, mice subjected to renal ischemia reperfusion injury had significantly lower levels of renalase in the plasma and kidney compared with sham-operated mice. Consistent with this, plasma NE levels increased significantly after renal ischemia reperfusion injury. Furthermore, renal tubular inflammation, necrosis, and apoptosis were more severe and plasma catecholamine levels were higher in renalasedeficient mice subjected to renal ischemia reperfusion compared with wild-type mice. Administration of recombinant human renalase reduced plasma catecholamine levels and ameliorated ischemic AKI in wildtype mice. Taken together, these data suggest that renalase protects against ischemic AKI by reducing renal tubular necrosis, apoptosis, and inflammation, and that plasma renalase might be a biomarker for AKI. Recombinant renalase therapy may have potential for the prevention and treatment of AKI.

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“…[9][10][11] On the other hand, it has also been indicated that sympathetic overactivity plays a pivotal role in the progression of renal disease in patients with chronic kidney disease and in experimental animals. [12][13][14][15] Therefore, it is expected that treatment aimed to modulate sympathetic nerve activity would be of benefit to renal tissue.…”

Section: Introductionmentioning

confidence: 99%

L/N-type calcium channel blocker cilnidipine ameliorates proteinuria and inhibits the renal renin–angiotensin–aldosterone system in deoxycorticosterone acetate-salt hypertensive rats

et al. 2011

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Cilnidipine, an N/L-type calcium channel blocker, has been reported to inhibit sympathetic nerve activity and has a greater renoprotective effect than L-type calcium channel blockers. To investigate the hypothesis that cilnidipine might ameliorate advanced hypertensive nephropathy and inhibit the renal renin-angiotensin-aldosterone system, cilnidipine (1 mg per kg per day) or amlodipine (1 mg per kg per day) was administered to uninephrectomized deoxycorticosterone (DOCA)-salt hypertensive rats (DOCA-salt) for 4 weeks by gavage. Although the blood pressure in the DOCA-salt group was higher than that of control, neither cilnidipine nor amlodipine had any effect on the increase in blood pressure in the DOCA-salt group. The DOCA (40 mg per kg per week, subcutaneously (s.c.)) and salt (1% NaCl in drinking water) treatment significantly aggravated the levels of urinary protein excretion and creatinine clearance and increased glomerulosclerosis and collagen deposition in the tubulointerstitial area of the kidney. These effects were attenuated by cilnidipine treatment. Reverse transcription-polymerase chain reaction analysis revealed that the renal expression of mRNA for collagen I/IV and transforming growth factor-b was enhanced in the DOCA-salt group and that the overexpression of these molecules was suppressed by cilnidipine. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived superoxide production in the kidney and urinary norepinephrine excretion, which were enhanced in the DOCA-salt group, were suppressed by cilnidipine. Cilnidipine also decreased the activity and expression of angiotensin-converting enzyme (ACE) and the aldosterone concentration in the renal homogenate. Although neither cilnidipine nor amlodipine had any effect on the increased blood pressure in the DOCA-salt group, these renal changes were not induced by treatment with amlodipine. In conclusion, cilnidipine inhibited renal dysfunction, sympathetic nerve activity and renal renin-angiotensin-aldosterone system in the DOCA-salt group.

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The role of renal sympathetic nervous system in the pathogenesis of ischemic acute renal failure

Cited by 105 publications

References 17 publications

Retraction：Dietary Supplementation of L-Carnosine Prevents Ischemia/Reperfusion-Induced Renal Injury in Rats

Retraction：Dietary Supplementation of L-Carnosine Prevents Ischemia/Reperfusion-Induced Renal Injury in Rats

Renalase Protects against Ischemic AKI

L/N-type calcium channel blocker cilnidipine ameliorates proteinuria and inhibits the renal renin–angiotensin–aldosterone system in deoxycorticosterone acetate-salt hypertensive rats

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