Blood flow and pressure pulsatility, which are present in vivo but not in vitro may explain why in vitro an increase in smooth muscle tone in response to phenylephrine (PHE) is associated to an increase in large artery compliance, whereas in vivo an increase in sympathetic tone determinates a decrease in large artery compliance. Our objective was to determine in vitro under conditions of smooth muscle activation and relaxation, the influence of pulse pressure (PP) on the visco-elastic properties of the abdominal aorta of the rat. Compliance (C) defining the elastic properties of the artery as a hollow structure, incremental elastic modulus (E i n c ) defining the stiffness of the arterial wall material, and aortic wall viscosity (AWV) calculated as the surface of the hysteresis of the pressure-volume curve. Rat abdominal aorta were isolated and perfused in an organ chamber. Arteries were submitted to various levels of PP (static condition 0 mmHg, dynamic conditions PP 20, 30, 40 and 50 mmHg), for each level of mean pressure (75, 100, 125 and 150 mmHg) under PHE and sodium nitroprusside (NPS). Pulse pressure waves similar to in vivo ones were generated by a pressure wave synthetizer. Pressure-diameter curves were determined from the simultaneous measurements of internal aortic diameter (high precision echotracking system NIUS), and aortic pressure (Millar probe 2F). After PHE and NPS, static compliance was higher than dynamic compliance (p<0.01), and static E i n c was lower than dynamic E i n c (p<0.01). Under static and dynamic conditions, for each level of mean pressure and PP, internal aortic diameter was lower under PHE than NPS (p<0.01), compliance was higher (p<0.05), Einc was lower (p<0.001) and AWV remained unchanged. These results indicate that, in vitro, an increase in smooth muscle tone is not accompanied by a decrease in arterial compliance, even when pulse pressure is pulsatile, but rather by an improvement of the elastic properties of the artery as a whole (C) and the arterial material (E i n c ). These results suggest that other factors than pulse pressure and AWV could explain why compliance is not increased, in vivo in response to sympathetic activation.