The expression and mRNA levels of eNOS are not compromised in hyperglycemia conditions but are inhibited by ROS and increased the availability of asymmetric dimethylarginine (ADMA); on the contrary, inducible nitric oxide synthase (iNOS) has an aberrant expression and activity, which leads to cardiomyocyte death due to caspase-3 nitrosylation and excitation-contraction uncoupling through myosin light chain (MLC) dysfunction and promotes cardiac wall stiffness, depletion of vasodilatation mechanisms, and diastolic dysfunction [21,25,27]. Here, NOS3 is linked to Hyperglycemia.