Role of endothelin in the pathophysiology of renal ischemia-reperfusion in normal rabbits
| Autor: | Gaudencio Espinosa, Enzo Digiuni, Carlos Caramelo, Dunyong Tan, M Montón, Inmaculada Millás, Juan R. Mosquera, María R. Cernadas, Santos Casado, Luis Hernando, Antonio López Farré, Félix Manzarbeitia |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Male
medicine.medical_specialty Neutrophils Ischemia Renal function Granulocyte Kidney Kidney Function Tests Leukocyte Count Organ Culture Techniques Internal medicine medicine Animals Peroxidase Endothelin-1 business.industry Flow Cytometry medicine.disease Endothelin 1 Pathophysiology Perfusion medicine.anatomical_structure Endocrinology Nephrology Reperfusion Injury Immunology Kidney Diseases Rabbits Endothelin receptor business |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 0085-2538 |
| DOI: | 10.1038/ki.1996.376 |
| Popis: | Role of endothelin in the pathophysiology of renal ischemia-reperfusion in normal rabbits. The present study addressed the acute effects of endothelin-1 on renal function and neutrophils accumulation in the setting of in vivo severe (60 min) acute ischemia/reperfusion. Ischemia/reperfusion decreased renal functional parameters and increased renal neutrophil accumulation and medullary congestion. All these parameters markedly improved with the intrarenal administration of anti-endothelin-1 antiserum. Comparatively, the intrarenal infusion of endothelin-1 decreased renal function and increased neutrophil accumulation. Abnormalities in renal histology were, however, less pronounced than with ischemia/reperfusion. In experiments using rabbit isolated perfused kidneys, endothelin-1 induced the accumulation of labeled neutrophils. This accumulation was similar to that observed in kidneys obtained after 60 minutes of ischemia plus 60 minutes of reperfusion. Both endothelin and ischemia/reperfusion effects were counteracted by an anti-endothelin antibody. In further in vitro studies, we found that endothelin-1-induced the expression of the CD 18 antigens on the neutrophil surface. In subsequent experiments based on this effect of ET-1 on CD18 antigens, a blockade of both ischemia/reperfusion-induced and endothelin-1-induced neutrophil accumulation was obtained by infusion an anti-CD18 antibody. In conclusion, our experiments disclosed the critical role of endothelin-1 as a major promoter of early neutrophil accumulation after ischemia/reperfusion, which occurred through an integrin-mediated mechanism. |
| Databáze: | OpenAIRE |
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