Structural changes of the arterial vasculature are of major pathophysiologic and prognostic significance in human hypertension. A high-resolution ultrasonic echotracking device was used to measure internal diameter and intima-media thickness of the radial artery, a medium-sized muscular conduit artery, in 60 hypertensive patients and in 40 agematched control subjects. Of the 60 hypertensives, 33 were never treated and 27 were well-controlled by antihypertensive therapy. Radial artery mass and thickness/radius ratio were used to describe the radial artery structure. Radial artery mass was validated in vitro by comparing the weight of arterial segments to the ultrasonographic determination of their mass, calculated as: ρ L(πRe2 − πRi2), where ρ is the arterial wall density, L the length of the arterial segment, and Re and Ri the ultrasonic values of internal and external radii, respectively. Diastolic internal diameter did not differ among the three groups, but wall thickness, radial artery mass, and thickness/radius ratio were significantly higher in the untreated hypertensive group than in the control group. In treated well-controlled hypertensive subjects, radial artery mass and thickness/radius ratio were not different from that of control subjects. Among the population of untreated patients, significant univariate relations existed between radial artery mass and blood pressure and radial artery mass and age. In multivariate analysis, radial artery mass was independently predicted by mean blood pressure, age, and sex. Circumferential wall stress, calculated from diastolic internal diameter, wall thickness, and diastolic blood pressure, was not different in the three groups. These results suggest that the increase in radial artery mass is a reaction to the high blood pressure according to the classic Laplace law. Long-term control of blood pressure might normalize radial artery wall thickness and radial artery mass. Longitudinal studies using this new approach are needed to evaluate the effects of antihypertensive therapy on vascular structure. Am J Hypertens 1994;7:1076–1084