Although the viscoelasticity of large arteries has been extensively investigated, few studies have focused on arterial wall viscosity (AWV) itself and its regulation by the endothelium in vivo. This is of particular importance since AWV is a major source of energy dissipation through the vascular system reducing the efficiency of cardiovascular coupling.
We simultaneously measured in 8 healthy volunteers (age: 22±1 years) radial artery diameter and arterial pressure (NIUS02) before and after 8min local infusion of L-NMMA (8mmol/min) as NO-synthase inhibitor, tetraethylammonium (TEA: 9mmol/ min), as blocker of calcium-activated potassium channels, the target of endothelium-derived hyperpolarizing factors (EDHF), and L-NMMA+TEA. Arterial pressure and diameter were carefully synchronized and the pressure-diameter relationship were constructed at each cardiac cycle. AWV was estimated from the ratio of the area of the hysteresis loop of the pressure-diameter relationship to the area representing the whole energy exchanged during each cardiac cycle (figure). Radial artery stiffness was evaluated during the whole cardiac cycle by the calculation of cross-sectional distensibility and during the ventricular ejection period by the slope of the ascending loop.
L-NMMA did not modify significantly arterial distensibility and ascending slope but, paradoxically reduced AWV (from 29.5±0.7 to 24.9±0.7 %, P=0.05). Conversely, TEA reduced arterial distensibility (from 6.50±0.19 to 5.53±0.2 10-5.kPa, P=0.002) and the ascending slope (from 1.03±0.01 to 0.86±0.03mm.mmHg, P<0.001) and increased AWV (from 29.1±0.5 to 35.0±0.7 %, P=0.04). The combination of L-NMMA+TEA induced a more marked decrease in distensibility (from 6.86±0.24 to 4.85±0.17 10-5.kPa, P<0.001) and ascending slope (from 1.06±0.04 to 0.69±0.03mm.mmHg, P<0.001) and increase in AWV (from 29.0±0.9 to 43.0±0.7, P=0.04) as compared with TEA alone (all P<0.05).
These results demonstrate in vivo in humans that the vascular endothelium contributes, in addition to large artery elasticity, to the regulation of AWV through the release of NO and EDHF