Aging was associated with a reduction of endothelium-dependent NO· signalling attested by the loss of the CCh-induced relaxation and the decrease of phosphorylation of eNOS and its upstream kinase Akt, in agreement with the role of Akt/eNOS signalling impairment in aging-induced endothelial dysfunction [20, 25]. Here, AKT1 is linked to endothelial dysfunction.