“…'Functional' mechanisms include a reduction in endothelial secretion of nitric oxide and a sympathetic activation [12,20,21], which is presumably followed by contraction of smooth muscle in the arterial wall and an increase of its elastic modulus compared to the relaxed state. Structural mechanisms include an increased synthesis of nondistensible tissue, such as collagen [22], as well as a vascular remodeling that increases wall thickness [13,23,24]. However, in the present study, the relationship between the decrease in AO Dist and the diseased coronary status persisted after adjustment from between-group differences, such as gender, age and systolic blood pressure.…”