Abstract
Arterioles in the cutaneous microcirculation frequently display an oscillatory phenomenon defined vasomotion, consistent with periodic diameter variations in the micro-vessels associated with particular physiological or abnormal conditions. The cellular mechanisms underlying vasomotion and its physiological role have not been completely elucidated. Various mechanisms were demonstrated, based on cell Ca2+ oscillations determined by the activity of channels in the plasma membrane or sarcoplasmic reticulum of vascular cells. However, the possible engagement in vasomotion of cell metabolic oscillations of mitochondrial or glycolytic origin has been poorly explored. Metabolic oscillations associated with the production of ATP energy were previously described in cells, while limited studies have investigated these fluctuations in-vivo. Here, we characterised a low-frequency metabolic oscillator (MO-1) in skin from live wild-type and Nrf2−/− mice, by combination of fluorescence spectroscopy and wavelet transform processing technique. Furthermore, the relationships between metabolic and microvascular oscillators were examined during phenylephrine-induced vasoconstriction. We found a significant interaction between MO-1 and the endothelial EDHF vasomotor mechanism that was reduced in the presence of oxidative stress (Nrf2−/− mice). Our findings suggest indirectly that metabolic oscillations may be involved in the mechanisms underlying endothelium-mediated skin vasomotion, which might be altered in the presence of metabolic disturbance.
Highlights
The term vasomotion indicates rhythmic oscillations of blood vessels diameter responsible for changes in the vascular tone and blood perfusion to tissue[1,2]
All this evidence suggests that the energetic and oxygen tissue requirements might stimulate vasomotion phenomena associated with Ca2+ oscillations of metabolic origin, which may involve the intercellular communication between heterogeneous groups of cells (e.g. endothelial cells (ECs), vascular smooth muscle cells (VSMCs) and cells of the tissue surrounding blood vessels)
Time resolution is scarce in the low frequencies, we clearly identified three heterogeneous oscillatory intervals defined metabolic oscillator-1 (MO-1) (5–9 × 10−3 Hz), metabolic oscillator-2 (MO-2) (2.5–5 × 10−3 Hz) and metabolic oscillator-3 (MO-3) (1.5–2.5 × 10−3 Hz)
Summary
The term vasomotion indicates rhythmic oscillations of blood vessels diameter responsible for changes in the vascular tone and blood perfusion to tissue[1,2]. A third hypothesised driving mechanism is the presence of a metabolic oscillator represented by oscillations in the activity of the glycolytic enzyme phosphofructokinase (PFK) that cause fluctuations in glycolysis, ATP levels and in the activity of plasma membrane ion channels and membrane potential[1] This mechanism has never been considered important because of limited experimental evidence for the involvement of PFK in glycolytic and Ca2+ fluctuations[1,2]. The external oxygen required for sustaining the electron transport chain has been proposed as the driving force for the mitochondrial oscillator[18] All this evidence suggests that the energetic and oxygen tissue requirements might stimulate vasomotion phenomena associated with Ca2+ oscillations of metabolic origin, which may involve the intercellular communication between heterogeneous groups of cells (e.g. ECs, VSMCs and cells of the tissue surrounding blood vessels)
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