It is unclear whether the stiffened arterial tree in systolic hypertension is the cause or the effect of the disease. In this study, brachial and radial arterial pulses were sensed by external Pixie transducers and measurements of pulse wave velocity converted to volume distensibility using the Bramwell-Hill equation. Blood pressure was controlled as a variable by repeating the measurements at a variety of transmural arterial pressures. This was accomplished by encasing the forearm in a rigid plastic cylinder within which pressures were varied. Twenty-nine patients with systolic hypertension were compared with 22 age-matched control subjects. At ambient pressures the volume distensibility of patients was lower than that of control subjects (0.10 versus 0.18% delta volume/mm Hg, p less than 0.001) but there was no difference in volume distensibility between the two groups at any comparable transmural pressure. Nineteen patients were treated for 1 month with a thiazide diuretic agent and the studies were then repeated. Systolic and diastolic blood pressure decreased significantly and volume distensibility increased (0.10 to 0.15% delta volume/mm Hg, p less than 0.001) at ambient pressures. But at comparable transmural pressures, volume distensibility was unchanged. It is concluded that, in the forearm, increased arterial stiffness is the result and not the cause of systolic hypertension, but these data cannot exclude increased aortic stiffness as a significant factor. Thiazide diuretic drugs increase forearm arterial compliance by lowering blood pressure without a demonstrable drug effect on this arterial wall.