In-vivo interaction of nitric oxide and endothelin

Abstract

The endothelin receptor expression pattern and the blood pressure responses to ETA and ETB receptor antagonists could not explain the lack of hypertension in ET-1 transgenic mice. Overexpression of the human ET-1 gene causes chronic kidney inflammation with an induction of vascular iNOS expression. The induction of iNOS expression might cause a new local balance between vascular ET-1 and nitric oxide, resulting in no alterations of blood pressure.