Dynamics of a three-variable nonlinear model of vasomotion: comparison of theory and experiment.

The effects of pharmacological interventions that modulate Ca(2+) homeodynamics and membrane potential in rat isolated cerebral vessels during vasomotion (i.e., rhythmic fluctuations in arterial diameter) were simulated by a third-order system of nonlinear differential equations. Independent control variables employed in the model were [Ca(2+)] in the cytosol, [Ca(2+)] in intracellular stores, and smooth muscle membrane potential. Interactions between ryanodine- and inositol 1,4,5-trisphosphate-sensitive intracellular Ca(2+) stores and transmembrane ion fluxes via K(+) channels, Cl(-) channels, and voltage-operated Ca(2+) channels were studied by comparing simulations of oscillatory behavior with experimental measurements of membrane potential, intracellular free [Ca(2+)] and vessel diameter during a range of pharmacological interventions. The main conclusion of the study is that a general model of vasomotion that predicts experimental data can be constructed by a low-order system that incorporates nonlinear interactions between dynamical control variables.