title: [Role of nitric oxide in the regulation of the mechanical properties of peripheral muscular arteries in man].
abstract: Although several experiments have demonstrated the existence of a basal NO-dependent vasodilatory tone at the arteriolar level, the contribution of NO to the mechanical properties of large arteries has not been investigated in humans. To evaluate the effect of NO-synthase inhibition on these mechanical properties, radial artery internal diameter (d, mm) and wall thickness (h, mm) were measured continuously in 11 healthy volunteers (age: 24 +/- 1 years), using an A-mode echo-tracking system 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 inhibitor of NO synthesis NG-monomethyl L-arginine (L-NMMA: 4 mumol/min for 5 min, infusion rate 0.8 ml/min). Arterial compliance C, 10(-3) mm2/mmHg), distensibility (D, 10(-3)/mmHg), mid-wall stress (sigma, 10(5) dynes/mm2) and incremental modulus (Ei, 10(7) dynes/mm2) 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): [table: see text] Thus, the L-NMMA-induced decrease in radial arterial wall stiffness (Ei) without changes in arterial diameter or stress demonstrates that NO-synthase inhibition induces an isometric relaxation of vascular muscle cells, which explains the increase of arterial compliance at constant mid-wall stress. These results demonstrate that NO contributes to the regulation of peripheral muscular arterial mechanics in humans. At the level of large arteries, the isometric relaxation observed after NO-synthase inhibition is probably the consequence of compensatory vasodilator mechanisms.
authors.affiliation: Service de phármacologie, VACOMED, IFRMP, CHU de Rouen.
authors.forename: R
authors.initials: R
authors.lastname: Joannides
authors.forename: W E
authors.initials: WE
authors.lastname: Haefeli
authors.forename: L
authors.initials: L
authors.lastname: Linder
authors.forename: T F
authors.initials: TF
authors.lastname: Lüscher
authors.forename: V
authors.initials: V
authors.lastname: Richard
authors.forename: C
authors.initials: C
authors.lastname: Thuillez
mesh_terms: D000328:Adult; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D003187:Compliance; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000502:physiology*; D017534:Radial Artery / Q000000981:diagnostic imaging / Q000502:physiology*; D014463:Ultrasonography; D019323:omega-N-Methylarginine
chemical_list: D004791:Enzyme Inhibitors; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D001120:Arginine
vernacular_title: Rôle du monoxyde d'azote dans la régulation des propriétés mécaniques des artères musculaires périphériques chez l'homme.