Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo

Circulation. 1995 Mar 1;91(5):1314-9. doi: 10.1161/01.cir.91.5.1314.


Background: Experimental evidence suggests that flow-dependent dilatation of conduit arteries is mediated by nitric oxide (NO) and/or prostacyclin. The present study was designed to assess whether NO or prostacyclin also contributes to flow-dependent dilatation of conduit arteries in humans.

Methods and results: Radial artery internal diameter (ID) was measured continuously in 16 healthy volunteers (age, 24 +/- 1 years) with a transcutaneous A-mode echo-tracking system coupled to a Doppler device for the measurement of radial blood flow. In 8 subjects, a catheter was inserted into the brachial artery for measurement of arterial pressure and infusion of the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA; 8 mumol/min for 7 minutes; infusion rate, 0.8 mL/min). Flow-dependent dilatation was evaluated before and after L-NMMA or aspirin as the response of the radial artery to an acute increase in flow (reactive hyperemia after a 3-minute cuff wrist occlusion). Under control conditions, release of the occlusion induced a marked increase in radial blood flow (from 24 +/- 3 to 73 +/- 11 mL/min; P < .01) followed by a delayed increase in radial diameter (flow-mediated dilatation; from 2.67 +/- 0.10 to 2.77 +/- 0.12 mm; P < .01) without any change in heart rate or arterial pressure. L-NMMA decreased basal forearm blood flow (from 24 +/- 3 to 13 +/- 3 mL/min; P < .05) without affecting basal radial artery diameter, heart rate, or arterial pressure, whereas aspirin (1 g PO) was without any hemodynamic effect. In the presence of L-NMMA, the peak flow response during hyperemia was not affected (76 +/- 12 mL/min), but the duration of the hyperemic response was markedly reduced, and the flow-dependent dilatation of the radial artery was abolished and converted to a vasoconstriction (from 2.62 +/- 0.11 to 2.55 +/- 0.11 mm; P < .01). In contrast, aspirin did not affect the hyperemic response nor the flow-dependent dilatation of the radial artery.

Conclusions: The present investigation demonstrates that NO, but not prostacyclin, is essential for flow-mediated dilatation of large human arteries. Hence, this response can be used as a test for the L-arginine/NO pathway in clinical studies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Arginine / analogs & derivatives
  • Arginine / pharmacology
  • Aspirin / pharmacology
  • Blood Pressure / drug effects
  • Epoprostenol / physiology*
  • Female
  • Forearm / blood supply
  • Heart Rate / drug effects
  • Humans
  • Hyperemia / physiopathology
  • Male
  • Nitric Oxide / antagonists & inhibitors
  • Nitric Oxide / physiology*
  • Radial Artery / diagnostic imaging
  • Radial Artery / physiology*
  • Regional Blood Flow / drug effects
  • Ultrasonography, Doppler
  • Vasodilation / physiology*
  • omega-N-Methylarginine


  • omega-N-Methylarginine
  • Nitric Oxide
  • Arginine
  • Epoprostenol
  • Aspirin