We have shown that in addition to compliance and distensibility, the analysis of the arterial distension (pulsatile diameter) via echotracking (ArtLab) provides information to discriminate the pressure-dependent and independent arterial stiffening. In the present study we evaluated these parameters in different hypertensive rat models. Mean, systolic, diastolic and pulse arterial pressure (AP) and the aortic diameter were recorded in 6 groups of pentobarbital anaesthetized rats: 20 week old spontaneously hypertensive rat (SHR), SHR treated with the NOS inhibitor L-NAME 6 mg/kg/day in drinking water (SHRLN), 50–60 week old SHR, DOCA-salt (uni-nephrectomized, deoxycorticosterone treated rats) and VDN (VitamineD+Nicotine treated rats); all were compared to their respective controls: Wistar-Kyoto (WKY) and Wistar normotensive rats. The diameter was comparable in all groups. Except in the DOCA-salt, increased stiffness index and decreased compliance, distensibility and distension were observed, indicating an aortic stiffening. When in each rat AP was decreased acutely by clonidine i.v., reaching the control rat values of AP, stiffness index, compliance and distensibility were more or less restored in SHR>old SHR=SHRLN>VDN; however the diameter distension wave (area under the curve adjusted to heart rate) was restored in SHR, partially in old SHR, but not in SHRLN and VDN (table). These data show, via the analysis of the aortic pulse diameter distension, that in SHRLN and VDN the increase in aortic stiffness is in part pressure-independent and due to arterial wall remodeling. The results are in line with previous structural vascular wall studies.