Atrial natriuretic peptide attenuation of renal ischemia–reperfusion injury after major surgery
Autor: | Yuichi Kanmura, Takahiro Moriyama, Sten G. E. Lindahl |
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Rok vydání: | 2016 |
Předmět: |
Male
0301 basic medicine medicine.medical_specialty Angiotensinogen Ischemia 030204 cardiovascular system & hematology Kidney Rats Sprague-Dawley 03 medical and health sciences chemistry.chemical_compound Oxygen Consumption Postoperative Complications 0302 clinical medicine Lipocalin-2 Atrial natriuretic peptide Proto-Oncogene Proteins Internal medicine medicine Animals Creatinine Renal ischemia business.industry Angiotensin II Acute kidney injury Acute Kidney Injury medicine.disease Lipocalins Mitochondria 030104 developmental biology Endocrinology medicine.anatomical_structure chemistry Reperfusion Injury Surgery business Reperfusion injury Atrial Natriuretic Factor Acute-Phase Proteins |
Zdroj: | Journal of Surgical Research. 201:213-218 |
ISSN: | 0022-4804 |
DOI: | 10.1016/j.jss.2015.10.036 |
Popis: | 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. Materials and 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. |
Databáze: | OpenAIRE |
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