The relationships between steady and pulsatile pressures, smooth muscl
e tone, and arterial viscoelastic behavior remain a matter of controve
rsy. We previously showed that arterial wall viscosity (AWV) was 3-fol
d lower in vivo than in vitro and suggested that in vivo active mechan
isms could minimize intrinsic AWV to improve the efficiency of heart-v
essel coupling energy balance. The aim of the present study was to det
ermine the role of smooth muscle tone on AWV, under various levels of
steady and pulsatile pressures, both in vivo and in vitro. AWV of rat
abdominal aorta was studied first in vivo after bolus injections of ph
enylephrine (PE) or sodium nitroprusside (SNP), then in vitro in respo
nse to PE or SNP. In vitro, arterial segments were submitted first to
steady pressure (0 to 200 mm Hg) by increments of 20 mm Hg, then to in
creasing levels of pulse pressure (20 to 50 mm Hg) at various mean art
erial pressures (75 to 150 mm Hg). AWV was quantified as the area of t
he pressure/diameter relationship hysteresis, issued from the simultan
eous measurements of pressure (Millar micromanometer) and diameter (NI
US echotracking device). In vivo, AWV increased after PE and decreased
after SNP, in parallel with pressure changes. In vitro, AWV was not s
ignificantly influenced by PE and SNP. After both PE and SNP, AWV incr
eased with pulse pressure but was not influenced by mean arterial pres
sure. At any given pulse pressure, AWV was higher in vitro than in viv
e. The relation between AWV and pulse pressure was significantly steep
er in vitro than in vive. These results show that AWV is strongly infl
uenced by steady and pulsatile mechanical load but not by smooth muscl
e tone, both in vive and in vitro. Factors other than sustained smooth
muscle activation should be explored to explain the minimization of A
WV in vive compared with intrinsic in vitro values.