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Effect of chronic inhibition of endothelin-1 receptor in cyclosporine induced nephrotoxicity in normotensive and hypertensive animals

Grant number: 15/22809-1
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): May 01, 2016
Effective date (End): December 31, 2016
Field of knowledge:Health Sciences - Medicine - Medical Clinics
Principal Investigator:Fernanda Teixeira Borges
Grantee:Bianca Castino
Home Institution: Pró-Reitoria de Pós-Graduação e Pesquisa. Universidade Cruzeiro do Sul (UNICSUL). São Paulo , SP, Brazil

Abstract

Cyclosporine-A is an immunosuppressive agent widely used for controlling various kinds of rejection in transplants, including kidney. However, its use is associated with acute and chronic nephrotoxic injury. Chronic toxicity associated with cyclosporin involves an increase in the resistance of afferent and efferent arterioles, decreased renal blood flow and glomerular filtration rate, renal interstitial fibrosis and loss of an organ. The increase in resistance induced by cyclosporine is associated with vasoconstrictive agents such as angiotensin 2.The two leading causes of chronic kidney disease, which can progress to dialysis or transplantation is diabetes and hypertension, which can increase the nephrotoxic effect of cyclosporin-A.The vasoconstricting agents produced in the kidneys include angiotensin 2 and endothelin-1, produced by glomerular endothelial cells and renal tubular. The endothelin-1 is involved in the development of fibrosis. The objective of this study is to evaluate the effect of chronic blockade of the endothelin-1 receptor in chronic kidney injury induced by cyclosporin-A genetically hypertensive rats.