Multiple Factors Influence Calcium Synchronization in Arterial Vasomotion

Abstract

The intercellular synchronization of spontaneous calcium (Ca2+) oscillations in individual smooth muscle cells is a prerequisite for vasomotion. A detailed mathematical model of Ca2+ dynamics in rat mesenteric arteries shows that a number of synchronizing and desynchronizing pathways may be involved. In particular, Ca2+-dependent phospholipase C, the intercellular diffusion of inositol trisphosphate (IP3, and to a lesser extent Ca2+), IP3 receptors, diacylglycerol-activated nonselective cation channels, and Ca2+-activated chloride channels can contribute to synchronization, whereas large-conductance Ca2+-activated potassium channels have a desynchronizing effect. Depending on the contractile state and agonist concentrations, different pathways become predominant, and can be revealed by carefully inhibiting the oscillatory component of their total activity. The phase shift between the Ca2+ and membrane potential oscillations can change, and thus electrical coupling through gap junctions can mediate either synchronization or desynchronization. The effect of the endothelium is highly variable because it can simultaneously enhance the intercellular coupling and affect multiple smooth muscle cell components. Here, we outline a system of increased complexity and propose potential synchronization mechanisms that need to be experimentally tested.