The causality between pathological ET-system activation and renal damage is supported by models where transgenic rodents expressing human ET-1 or endothelin 2 (ET-2) genes predominately in the kidney develop glomerulosclerosis, tubulointerstitial fibrosis, and renal insufficiency in the absence of systemic hypertension [9,10]. This evidence concerns the gene EDN2 and glomerulosclerosis.