Vasomotion is the oscillation of vascular tone with frequencies in the range from 1 to 20 min⁻¹ seen in most vascular beds. The oscillation originates in the vessel wall and is seen both in vivo and in vitro.

Recently, our ideas on the cellular mechanisms responsible for vasomotion have improved. Three different types of cellular oscillations have been suggested. One model has suggested that oscillatory release of Ca²⁺ from intracellular stores is important (the oscillation is based on a cytosolic oscillator). A second proposed mechanism is an oscillation originating in the sarcolemma (a membrane oscillator). A third mechanism is based on an oscillation of glycolysis (metabolic oscillator). For the two latter mechanisms, only limited experimental evidence is available.

To understand vasomotion, it is important to understand how the cells synchronize. For the cytosolic oscillators synchronization may occur via activation of Ca²⁺‐sensitive ion channels by oscillatory Ca²⁺ release. The ensuing membrane potential oscillation feeds back on the intracellular Ca²⁺ stores and causes synchronization of the Ca²⁺ release. While membrane oscillators in adjacent smooth muscle cells could be synchronized through the same mechanism that sets up the oscillation in the individual cells, a mechanism to synchronize the metabolic‐based oscillators has not been suggested.

The interpretation of the experimental observations is supported by theoretical modelling of smooth muscle cells behaviour, and the new insight into the mechanisms of vasomotion has the potential to provide tools to investigate the physiological role of vasomotion.