Abstract--Damping is the conversion of mechanical energy of a structure into thermal energy, and it is related to the material viscous behavior. To evaluate the role of damping in the common carotid artery (CCA) wall in human hypertension and the possible improvement of angiotensin-converting enzyme (ACE) inhibition, we used noninvasive CCA pressure (tonometry) and diameter (B-mode echography) waveforms in normotensive subjects (NT group; n=12) and in hypertensive patients (HT group; n=22) single-blind randomized into HT-placebo (n=10) or HT-treated (ramipril, 5 to 10 mg/d during 3 months; n=12). Vascular smooth muscle (VSM) null tonus condition was achieved from in vitro pressure and diameter waveforms (Konigsberg microtransducer and sonomicrometry) measured in explanted human CCA (n=14). Arterial wall dynamics was described by viscous (), inertial (M), and compliance (C) parameters, mean circumferential wall stress, viscous energy dissipation (W_D), peak strain energy (W_St), damping ratio (=W_D/W_St), and modeling isobaric indexes C_Iso and W_St(Iso). The lack of VSM tonus isobarically increased wall stress and reduced , C_Iso, and damping (P<0.01). Wall stress, , and W_D were greater in HT than in NT (P<0.015) and arrived near normal in HT-treated (P<0.032 respect to HT), with no changes in HT-placebo. Whereas C_Iso increased in HT-treated (P<0.01) approaching the NT level, did not vary among groups. During hypertension, because of the W_St increase, the arterial wall reacts increasing W_D to maintain . ACE inhibition modulates VSM activation and vessel wall remodeling, significantly improving wall energetics and wall stress. This protective vascular action reduces extra load to the heart and maintains enhanced arterial wall damping.