ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2017
Endothelin-1 receptor antagonists protect the kidney against the nephrotoxicity induced by cyclosporine-A in normotensive and hypertensive rats.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 21 citations in OpenAlex.
- Heterogeneity in the efficacy of bosentan for hypertensive nephropathy: a study on individualized benefit prediction models based on pathological subtyping and dynamic trajectories.Annals of medicine · 2026Article
- Endothelin Receptor Antagonists in Kidney Disease.International journal of molecular sciences · 2023Review
- 2-Methoxyestradiol TPGS Micelles Attenuate Cyclosporine A-Induced Nephrotoxicity in Rats through Inhibition of TGF-β1 and p-ERK1/2 Axis.Antioxidants (Basel, Switzerland) · 2022Article
- Consideration of Metabolite Efflux in Radiolabelled Choline Kinetics.Pharmaceutics · 2021Article
- Ameliorative role of bosentan, an endothelin receptor antagonist, against sodium arsenite-induced renal dysfunction in rats.Environmental science and pollution research international · 2021Article
- The challenge of managing comorbidities: a case report of primary Sjogren's syndrome in a patient with acute intermittent porphyria.Intractable & rare diseases research · 2020Article
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10 authors at 4 institutions in 1 country.
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Abstract
Cyclosporin-A (CsA) is an immunosuppressant associated with acute kidney injury and chronic kidney disease. Nephrotoxicity associated with CsA involves the increase in afferent and efferent arteriole resistance, decreased renal blood flow (RBF) and glomerular filtration. The aim of this study was to evaluate the effect of Endothelin-1 (ET-1) receptor blockade with bosentan (BOS) and macitentan (MAC) antagonists on altered renal function induced by CsA in normotensive and hypertensive animals. Wistar and genetically hypertensive rats (SHR) were separated into control group, CsA group that received intraperitoneal injections of CsA (40 mg/kg) for 15 days, CsA+BOS and CsA+MAC that received CsA and BOS (5 mg/kg) or MAC (25 mg/kg) by gavage for 15 days. Plasma creatinine and urea, mean arterial pressure (MAP), RBF and renal vascular resistance (RVR), and immunohistochemistry for ET-1 in the kidney cortex were measured. CsA decreased renal function, as shown by increased creatinine and urea. There was a decrease in RBF and an increase in MAP and RVR in normotensive and hypertensive animals. These effects were partially reversed by ET-1 antagonists, especially in SHR where increased ET-1 production was observed in the kidney. Most MAC effects were similar to BOS, but BOS seemed to be better at reversing cyclosporine-induced changes in renal function in hypertensive animals. The results of this work suggested the direct participation of ET-1 in renal hemodynamics changes induced by cyclosporin in normotensive and hypertensive rats. The antagonists of ET-1 MAC and BOS reversed part of these effects.
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