1. The mechanism of postural vasoconstriction in the skin of the foot was examined in 102 healthy subjects by using laser Doppler flowmetry.
2. In 45 subjects, when one foot was lowered 50 cm below heart level and the other foot kept horizontal, blood flow was progressively reduced in the dependent foot (by 79%) with a concomitant, but less pronounced, reduction in flow in the horizontal foot (by 18%), indicating that a central mechanism is involved. After lumbar sympathetic blockade (in 10 patients with epidural anaesthesia), the flow in the horizontal foot remained virtually constant, indicating that the central component is mainly mediated via efferent sympathetic nerves, whereas the postural fall in flow in the dependent foot, though partially attenuated, was preserved, indicating that a local mechanism is mainly involved.
3. On lowering one foot below heart level in 12 subjects, there was a small but significant reduction in systolic and mean arterial pressures during the first minute of dependency. During the fourth minute, systolic pressure decreased, diastolic pressure and heart rate increased, but the mean arterial pressure was maintained.
4. In 19 subjects postural vasoconstriction was nearly abolished during local nervous blockade (lignocaine 3.7 × 10−4–7.4 × 10−2 mol/l), indicating that the local mechanism mediating the vasoconstriction is mainly neurogenic in nature. However, there was still a small fall (19%) in flow in the dependent foot during blockade, probably indicating a minor contribution of a local myogenic mechanism.
5. In three subjects, application of venous occlusion of 40 mmHg with the foot at heart level reduced the flow by 63% at rest, and by only 12% during local nervous blockade, indicating that the increased venous pressure on dependency provides the main stimulus for postural vasoconstriction. However, a greater reduction in flow was observed in 13 subjects when the foot was lowered 50 cm below the heart (75%) than during venous occlusion of 40 mmHg (52%) with foot at heart level, indicating that not only the increase in venous pressure but also the increase in arterial transmural pressure is implicated in the postural increase in precapillary resistance.
6. It is concluded that postural vasoconstriction in the human foot is mainly produced by a local neurogenic mechanism with a small contribution from a local myogenic response, in addition to a centrally elicited sympathetic component.