Rapid versus slow ascending vasodilatation: intercellular conduction versus flow-mediated signalling with tetanic versus rhythmic muscle contractions.

key pointsIn response to exercise, vasodilatation ascends from downstream arterioles into upstream feed arteries (FAs). We hypothesized that the signalling events underlying ascending vasodilatation variy with the intensity and duration of skeletal muscle contraction. In the gluteus maximus muscle of C57BL/6 mice, brief tetanic contraction evoked rapid onset vasodilatation (ROV) (<1 s) throughout the resistance network. Selective damage to endothelium midway between FAs and primary arterioles eliminated ROV only in FAs. Blocking SK ABSTRACT: In response to exercise, vasodilatation initiated within the microcirculation of skeletal muscle ascends the resistance network into upstream feed arteries (FAs) located external to the tissue. Ascending vasodilatation (AVD) is essential for reducing FA resistance that otherwise restricts blood flow into the microcirculation. In the present study, we tested the hypothesis that signalling events underlying AVD vary with the intensity and duration of muscle contraction. In the gluteus maximus muscle of anaesthetized male C57BL/6 mice (aged 3-4 months), brief tetanic contraction (100 Hz for 500 ms) evoked rapid onset vasodilatation (ROV) in FAs that peaked within 4 s. By contrast, during rhythmic twitch contractions (4 Hz), slow onset vasodilatation (SOV) of FAs began after ∼10 s and plateaued within 30 s. Selectively damaging the endothelium with light-dye treatment midway between a FA and its primary arteriole eliminated ROV in the FA along with conducted vasodilatation of the FA initiated on the arteriole using ACh microiontophoresis. Superfusion of SK