EFFECTS OF NITRIC-OXIDE SYNTHASE INHIBITI ON ON THE MECHANICAL-PROPERTIES OF MUSCULAR ARTERIES IN HUMANS

Although several experiments have demonstrated the existence of a basa l NO-dependent vasodilatory tone at the arteriolar level, the contribu tion of NO to the mechanical properties of large arteries has not been investigated in humans. To evaluate the effect of NO-synthase inhibit ion on these mechanical properties, radial artery internal diameter (d , mm) and wall thickness (h, mm) were measured continuously in 11 heal thy volunteers (age : 24 +/- 1 years), using an A-mode echo-tracking s ystem coupled to a Doppler device for the measurement of radial blood flow (RBF, ml/min). A catheter was inserted in the brachial artery for measurement of arterial pressure (AP, mmHg), and infusion of the inhi bitor of NO synthesis N-G-monomethyl L-arginine (L-NMMA : 4 mu mol/min for 5 min, infusion rate 0.8 ml/min). Arterial compliance C, 10(-3) m m(2)/mmHg), distensibility (D, 10(-3)/mmHg), mid-wall stress (sigma, 1 0(5) dynes/mm(2)) and incremental modulus (Ei, 10(7) dynes/mm(2)) were calculated before and after L-NMMA. After L-NMMA, RBF decreased from 31 +/- 6 to 23 +/- 4 (p < 0.05), radial vascular resistance increased from 2.70 +/- 0.35 to 3.77 +/- 0.55 (p < 0.05), without changes in AP or heart rate. Table shows mechanical parameters, assessed at fixed AP (80 mmHg) ( : p < 0.05 vs baseline): [GRAPHICS] Thus, the L-NMMA-ind uced decrease in radial arterial wall stiffness (Ei) without changes i n arterial diameter or stress demonstrates that NO-synthase inhibition induces an isometric relaxation of vascular muscle cells, which expla ins the increase of arterial compliance at constant mid-wall stress. T hese results demonstrate that NO contributes to the regulation of peri pheral muscular arterial mechanics in humans. At the level of large ar teries, the isometric relaxation observed after NO-synthase inhibition is probably the consequence of compensatory vasodilator mechanisms.