Several studies have shown that a rapid hyperaemia can be evoked by different stimuli such as short-lasting contractions, muscle compression, arterial occlusion and passive movement (Turturici et al. 2012, Kirby et al. 2007), suggesting that a rapid dilatation could be mediated by mechano-sensitive mechanisms responding to decreases in transmural pressure according to the Bayliss effect (Mohrman & Sparks 1974, Turturici et al. 2012). However the exact nature of the relevant mechanical stimulus is still unclear, given that these stimuli produce both a rapid decrease and rapid return of transmural pressure. Aim of this study was to investigate the individual effects of these two events by analysing the hemodynamic responses to onset and release of muscle compression. Hyperaemic responses to the external compression of Masseter muscle (MC) were recorded from the masseteric artery (n=8) of urethane-anaesthetized rabbits (1.2 g/kg, i.v.) (n=4) by means of ultrasound flowmetry. Mechanical compressions of different duration (1, 10, 20, 50 and 100 s) were exerted by a cylindrical head (1.3 cm^2) pushed by a PC-driven servo-controlled motor (force= 0.9 N) resulting in a locally generated pressure of about 50 mmHg (Turturici et al. 2013).The relative amplitude of the hyperaemic responses was computed as (peak flow – baseline)*100/baseline. MC did not substantially impair muscle blood flow. On the contrary, two different hyperaemic responses were detected both at the onset and release of MCs (with MC duration >= 10 s) of amplitude Po and Pr, respectively (see Fig. 1). None of these responses depended on MC duration p=(0,94). Po and Pr were not significantly different .Po=240±60% and Pr= 229±80% (averaged over all MC durations 10-100 s). The 1-s lasting MC evoked a single hyperaemic response whose amplitude (394 ± 124 % ) was of significantly higher than both Po and Pr. In conclusion, rapid release of MC consistently evokes a rapid dilatation. MC does not stop blood flow to the muscle and the hyperaemia does not increase with MC duration, suggesting that metabolic mechanisms are not involved. It is suggested that the rapid dilatation underlying the hyperaemia can be mechanically-activated by both a rapid decrease and a rapid increase in transmural pressure of the musculo-vascular network. This particular manifestation of vascular mechanosensitivity is not explained by the classical myogenic response but is compatible with the dilatory effects reported by Smiesko et al (1971) in the isolated skeletal muscle.