It was demonstrated using a mouse experimental model that NO decreases vasoconstrictor response to activation of α-adrenergic receptors, and therefore has a critical role in the blood flow regulation in exercising skeletal muscle and also in DMD in case of which the lack of nNOS causes unopposed sympathetic vasoconstriction that can contribute to muscle fiber apoptosis or necrosis [118,119]. The gene discussed is NOS1; the disease is Duchenne muscular dystrophy.