Calcitriol attenuates vascular remodeling in association with alteration of ppET-1/ETR/eNOS and ETR expression in acute and chronic phases of kidney ischemia-reperfusion injury in mice.

Kidney ischemia-reperfusion injury (IRI) causes acute kidney injury with increasing risk of maladaptive repair through endothelin-1 (ET-1)/endothelin type A receptor (ETR) signaling. Calcitriol shows renoprotection in kidney fibrosis, however, its effects on vasoactive substances expression and vascular remodeling following kidney IRI remain unclear. This research aimed to investigate Calcitriol's effects on preproendothelin-1 (), , endothelial nitric oxide synthase () mRNA expression and vascular remodeling in acute and chronic phases of kidney IRI in mice.