Key result
Nonpeptide endothelin antagonists bosentan and Ro 48-5695 did not prevent proteinuria or progression of glomerular sclerosis in rats with reduced renal mass, despite moderate antihypertensive effects.
Why the study?
Do nonpeptide endothelin receptor antagonists prevent or reverse renal damage and hypertension in rats with reduced renal mass?
Population
Rats with renal mass reduction (RMR)
Comparison
Bosentan for 14 weeks or Ro 48-5695 for 8 weeks vs Cilazapril for 14 weeks
Design
Preclinical
Follow-up
Up to 14 weeks
Authors
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Nonpeptide ET antagonists lack renoprotective effects in reduced renal mass rats; leaves open their role in other CKD models or humans.
Do nonpeptide endothelin receptor antagonists prevent or reverse renal damage and hypertension in rats with reduced renal mass?
Endothelin receptor antagonists do not prevent the progression of glomerular sclerosis in rats with reduced renal mass, suggesting ET activation is not a major driver of renal structural damage in this model.
Clozel et al. (1999) studied Renal mass reduction (chronic renal failure). Nonpeptide endothelin antagonists (bosentan, Ro 48-5695) vs. Cilazapril (10 mg/kg/day) or untreated was evaluated on Development of hypertension, proteinuria, and renal structural damage. Nonpeptide endothelin antagonists bosentan and Ro 48-5695 did not prevent proteinuria or progression of glomerular sclerosis in rats with reduced renal mass, despite moderate antihypertensive effects.
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