The effects of pharmacological interventions that modulate Ca2+ 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 [Ca2+] in the cytosol, [Ca2+] in intracellular stores, and smooth muscle membrane potential. Interactions between ryanodine- and inositol 1,4,5-trisphosphate-sensitive intracellular Ca2+ stores and transmembrane ion fluxes via K+ channels, Cl− channels, and voltage-operated Ca2+ channels were studied by comparing simulations of oscillatory behavior with experimental measurements of membrane potential, intracellular free [Ca2+] 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.
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