In the present study, we did not investigate the possible contribution of hypoalbuminemia to the reduced bioavailability of NO, but again the maintained levels of plasma NO2− + NO3−, together with the loss of bradykinin-induced NO-mediated vasodilation in buffer-perfused coronary small arteries, suggests that the loss of NO-mediated vasodilator influence occurred principally in the coronary microvascular endothelium. This evidence concerns the gene KNG1 and Hypoalbuminemia.