We observed normal endothelial function in uremic vessels, which is in concordance with earlier studies reporting preserved endothelium-dependent relaxation in uremic resistance vessels.[32–34] Decreased endothelium-dependent relaxation, however, has also been reported, caused by an impaired endothelium-derived hyperpolarizing factor (EDHF) response.[35, 36] From our data, it can be concluded that endothelial function is not severely compromised in carotid arteries in CKD, in contrast with SMC function that was clearly diminished due to NO resistance of the NO-receptor sGC. This evidence concerns the gene SGCB and chronic kidney disease.