Endothelium-derived nitric oxide regulates arterial elasticity in human arteries in vivo

Arterial elasticity is determined by structural characteristics of the arte ry wall and by vascular smooth muscle tone. The identity of endogenous vaso active substances that regulate elasticity has not been defined in humans. We hypothesized that NO, a vasodilator released constitutively by the endot helium, augments arterial elasticity. Seven healthy young men were studied. A 20-MHz intravascular ultrasound catheter was introduced through an arter ial sheath to measure brachial artery cross-sectional area, wall thickness, and intra-arterial pressure. After control was established, indices of ela sticity (pressure-area relationship, instantaneous compliance, and stress-s train, pressure-incremental elastic modulus (E-inc), and pressure-pulse wav e velocity relationships) were examined over 0 to 100 mm Hg transmural pres sure obtained by inflation of an external cuff. Thereafter, the basal produ ction of endothelium-derived NO was inhibited by N-G-monomethyl-L-arginine (L-NMMA) (4 and 8 mg/min). Finally, nitroglycerin (2.5 and 12.5 mug/min), a n exogenous donor of NO, was given to relax the vascular smooth muscle. Ela sticity was measured under all of these conditions. L-NMMA (8 mg/min) decre ased brachial artery area (P=0.016) and compliance (P <0.0001) and increase d E-inc (P <0.01) and pulse wave velocity (P <0.0001). Nitroglycerin (12.5 mug/min) increased brachial artery area (P <0.001) and compliance (P <0.001 ) and decreased pulse wave velocity (P=0.02). NO, an endothelium-derived va sodilator, augments arterial elasticity in the human brachial artery. Loss of constitutively released NO associated with cardiovascular risk factors m ay adversely affect arterial elasticity in humans.