Pain is regarded as a risk factor in pressure ulcer development by contributing to immobility. Pressure-induced vasodilatation (PIV) is a mechanism whereby cutaneous blood flow increases in response to progressive locally applied pressure, thereby delaying the occurrence of ischaemia and appearing to be a protective response to local pressure. When the interaction between nervous and vascular systems is deregulated, PIV, which relies on both systems, is absent. We thus hypothesized that acute pain could alter PIV. This study investigated the effects on PIV of acute pain triggered by noxious heat (50 degrees C) applied to the tail of anaesthetized rats. To address the mechanisms underlying these effects, chronic sympathectomy was performed using guanethidine, and the plasma concentrations of pituitary adrenocorticotrophin (ACTH) and catecholamines were measured. Our results show that acute pain induces a loss of PIV associated with an increase of ACTH. Direct involvement of hypertensive effects and peripheral sympathetic nervous system are excluded in the loss of PIV, whereas the activation of brain structures that have descending inhibitory control cannot be excluded. A low dose of systemic morphine prevented this loss of PIV and maintained the ability of the cutaneous microcirculation to adapt to the applied pressure. The loss of a protective response to local pressure (PIV) induced by acute pain lends physiological support to the direct involvement of pain in pressure ulcer development. Therefore, an adequate evaluation and treatment of pain is crucial.