Role of the myogenic mechanism in the genesis of microvascular oscillations (vasomotion): analysis with a mathematical model.

The possibility that spontaneous oscillations in microvessel caliber, called vasomotion, arise from the activity of the local myogenic mechanism is analyzed in this work using an original mathematical model. According to experimental results, the model assumes that the myogenic response in microcirculation (transverse arterioles and terminal precapillary-postcapillary microvessels) is characterized by both a static and a dynamic (i.e., rate-dependent) component. Computer simulations demonstrate that the myogenic mechanism of action, thanks to its strong rate-dependent component in terminal arterioles, can produce vascular instability and oscillations of vessel caliber without the need to assume the existence of a local pacemaker in smooth muscle cells. Moreover, these oscillations turn out similar, both in frequency and in shape, to those experimentally observed in microvascular networks. Finally, according to experimental data, several kinds of vasodilatory stimuli (such as arterial hypotension, increase in the tissue metabolic rate, and postischemic reactive hyperemia) cause stoppage of vasomotion and stabilization of vessel caliber.