In an effort to determine whether arterial conductance vessels dilate in response to increased blood flow stimuli, brachial artery area (cm2) and diameter (cm) were derived by simultaneous measurement of forearm blood flow (ml/min-100 ml) and brachial artery blood flow velocity (cm/sec) following the release of arterial occlusion. Measurements were made at rest and at the time of maximal flow after the release of graded periods of forearm arterial occlusion (20 seconds to 10 minutes). These studies showed a graded large vessel dilation following occlusions of up to 1 minute (baseline diameter, 0.33±0.01; after 1 minute occlusion, 0.45±0.02 cm; P<0.05) after which time diameter plateaued (after 10 minutes of occlusion, 0.48±0.02 cm). In addition, the tune course of diameter and flow changes after 3 minutes of arterial occlusion were examined. Flow was maximal at 5 seconds but diameter was maximal at 15-30 seconds after release. Furthermore, the half time for the return of diameter to baseline was longer than that for blood flow. We also measured the diameter after forearm heating (42°C) and noted a substantial increase in diameter (before heating, 0.32±0.01; after heating, 0.39±0.02 cm; p<0.05). Finally, we applied pressure to the venous side of arteriovenous fistnlae in five hemodialysis patients. This maneuver was associated with large reductions hi forearm blood flow (baseline flow, 63.3±10.6; venous compression flow, 36.0±4.4 ml/min 100 ml;p<0.05) and a decrease in brachial artery size (baseline diameter, 0.63±0.07; venous compression diameter, 0.58±0.06 cm; p<0.05). We conclude that 1) the human brachial artery size changes in response to changes in blood flow, and 2) the maximal dilation occurs after maximal flow is noted. Although alternate explanations are possible for each of our observations, our results are most consistent with a flow-mediated, localized vasodilating process.