Turturici M, Mohammed M, Roatta S. Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds. J Appl Physiol 113: 524 -531, 2012. First published June 7, 2012 doi:10.1152/japplphysiol.00237.2012.-Several mechanisms have been hypothesized to contribute to the rapid hyperemia at the onset of exercise. The aim of the present study was to investigate the role played by the mechanosensitivity of the vascular network. In 12 anesthetized rabbits blood flow was recorded from the exclusively muscular masseteric artery in response to brief spontaneous contractions (BSC) of the masseter muscle, artery occlusion (AO), muscle compression (MC), and muscle stretch (MS). Activation of masseter muscle was monitored by electromyography (EMG). Responses to AO were also recorded from the mostly cutaneous facial and the central ear arteries. Five animals were also tested in the awake condition. The hyperemic response to BSC (peak amplitude of 394 Ϯ 82%; time to peak of 1.8 Ϯ 0.8 s) developed with a latency of 300 -400 ms from the beginning of the EMG burst and 200 -300 ms from the contractioninduced transient flow reduction. This response was neither different from the response to AO (peak amplitude ϭ 426 Ϯ 158%), MC, and MS (P ϭ 0.23), nor from the BSC response in the awake condition. Compared with the masseteric artery, the response to AO was markedly smaller both in the facial (83 Ϯ 18%,) and in the central ear artery (68 Ϯ 20%) (P Ͻ 0.01). In conclusion, the rapid contractioninduced hyperemia can be replicated by a variety of stimuli affecting transmural pressure in muscle blood vessels and is thus compatible with the Bayliss effect. This prominent mechanosensitivity appears to be a characteristic of muscle and not cutaneous vascular beds. muscle stretch; myogenic response; rapid dilatation; reactive hyperemia; muscle compression SKELETAL MUSCLE BLOOD FLOW has long been known to exhibit a rapid increase at the onset of exercise (1,9,12,22,27). The mechanisms behind this phenomenon are still a matter of debate despite the many new insights provided by different research groups in recent years. In particular it has been shown that the contraction-induced compression of venous compartments (muscle pump) cannot fully account for the blood flow increase and that the additional occurrence of a rapid active dilatation is required (18,33,45,46). Other studies have shown that this rapid dilatation is mediated neither by changes in sympathetic neural drive (7, 41), nor by ACh spillover from the motor endplate (6, 33), nor by endothelium-released NO (6), although this last assertion is debated (see DISCUSSION). As early as 1974, Mohrman and Sparks (31) hypothesized that the rapid dilatation could result from the myogenic response of muscle blood vessels to decreased transmural pressure, which in turn results from the increase in intramuscular (extravascular) pressure produced by the contraction. They showed, in fact, that the rapid hypere...