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The myogenic tone and thus diameter of brain arterioles varies on multiple time scales. These variations result from coordinated contraction and relaxation of electrically coupled smooth muscle cells in the arteriole wall that drive constriction. A prominent feature is a broad-band ∼0.1 Hz rhythmicity, designated vasomotion, in the pial arterioles spanning the cortical mantle and the penetrating arterioles that nourish the capillary bed. As characterized in the murine brain, vasomotion supports propagating waves with a typical wavelength of 20 mm (a speed of 2 mm/s) that modulate perfusion with a magnitude equal to that of functional hyperemia. The spectral and spatial properties reflect the interaction of smooth muscle dynamics with the underlying neuronal drive. Possible functional roles of vasomotion are to mitigate capillary stalls and to facilitate the exchange of solutes between interstitial and cerebrospinal fluid. Indeed, loss of vasomotion has been implicated in the pathophysiology of vascular disease, such as cerebral amyloid angiopathy.
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Earley et al. (2026) studied this question.
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