This could be ascribed to NO resistance of the NO-receptor sGC as shown by an increased vasorelaxation of uremic vessels to BAY 60–2770, an activator of sGC, that exhibits an optimal effect when the heme group of sGC is oxidized or absent.[26, 31] In accordance, incubation with the very potent oxidizing agent ODQ, increased the sensitivity of control vessels to BAY 60–2770, but not uremic vessels, confirming that sGC is maximally oxidized in CKD. Here, SGCB is linked to chronic kidney disease.