title: Atrial natriuretic peptide attenuation of renal ischemia-reperfusion injury after major surgery.
abstract: BACKGROUND
  Ischemia-reperfusion (I/R) injury is one of the most important pathologic processes causing acute kidney injury. Human atrial natriuretic peptide (hANP) has various effects, including renal protection. The purpose of the present work was to study the effects of intrarenal angiotensin II (Ang II) and investigate the potential of hANP to prevent kidney injury.
  
  
  METHODS
  Male Sprague-Dawley rats were divided into three groups as follows: (1) sham; (2) I/R (30 min of bilateral renal ischemia followed by 6 h reperfusion); and (3) I/R + hANP (I/R injury + continuous intravenous infusion of hANP at 0.025 μg/kg/min). After 6 h of reperfusion, both renal and plasma Ang II concentrations were measured. Urinary angiotensinogen and neutrophil gelatinase-associated lipocalin were measured before ischemia and 2, 4, and 6 h after reperfusion. To evaluate the renal-protective effects of hANP, serum creatinine was determined 6 and 24 h after reperfusion. In addition, mitochondrial oxygen consumption in kidney cortex was measured in the presence of Ang II and hANP.
  
  
  RESULTS
  Renal Ang II concentrations were 24.5 ± 3.9 and 14.2 ± 3.4 pg/mg renal weight in the I/R and I/R + hANP groups, respectively. Urinary angiotensinogen and neutrophil gelatinase-associated lipocalin excretions were elevated after I/R injury. Treatment with hANP significantly attenuated this effect after 4 and 6 h. Oxygen consumption in renal mitochondria increased with the addition of Ang II, which was also attenuated by hANP.
  
  
  CONCLUSIONS
  Production of intrarenal Ang II was attenuated by hANP, indicating a potential to diminish renal I/R injury.
authors: Department of Anesthesiology and Intensive Care, Kagoshima University Hospital, Kagoshima, Japan. Electronic address: takmor@m3.kufm.kagoshima-u.ac.jp.
authors: Takahiro
authors: T
authors: Moriyama
authors: Department of Anesthesiology and Intensive Care, Kagoshima University Hospital, Kagoshima, Japan.
authors: Yuichi
authors: Y
authors: Kanmura
authors: Section of Anesthesiology and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
authors: Sten G E
authors: SG
authors: Lindahl
mesh_terms: D058186:Acute Kidney Injury / Q000378:metabolism / Q000517:prevention & control*; D000209:Acute-Phase Proteins / Q000652:urine; D000804:Angiotensin II / Q000378:metabolism*; D000808:Angiotensinogen / Q000652:urine; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000627:therapeutic use*; D007668:Kidney / Q000378:metabolism; D000071068:Lipocalin-2; D054834:Lipocalins / Q000652:urine; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D010101:Oxygen Consumption; D011183:Postoperative Complications / Q000378:metabolism / Q000517:prevention & control*; D011518:Proto-Oncogene Proteins / Q000652:urine; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*
chemical_list: D000209:Acute-Phase Proteins; C097278:Lcn2 protein, rat; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins; D000808:Angiotensinogen; D000804:Angiotensin II; D009320:Atrial Natriuretic Factor
keywords: Acute kidney injury; Atrial natriuretic peptide; Intrarenal angiotensin II; Ischemia–reperfusion; Mitochondria; Oxygen consumption