抄録
To elucidate the roles of intracellular Ca2+ dynamics in sinoatrial (SA) node pacemaking, we investigated the effects of SR Ca2+ cycling dynamics on bifurcation structures of mathematical models for the rabbit SA node cells. Modified versions of our model (Kurata et al. Am J Physiol, 2002) with various SR Ca2+ uptake and release rates were used. Equilibrium points (EPs), periodic orbits, stability of EPs, and bifurcation points were calculated for the model cells during changes in bifurcation parameters. Structural stability to applications of constant bias currents (Ibias) or hyperpolarizing loads was also evaluated. In all the model cells, blocking L-type Ca2+ current (ICa,L) caused EP stabilization and cessation of pacemaking via a Hopf bifurcation, and the unstable EP region determined with Ibias applications shrunk and finally disappeared as ICa,L diminished. All the model cells exhibited essentially the same bifurcation structures, regardless of whether or not intracellular Ca2+ dynamics significantly affects the action potential dynamics. Changing SR Ca2+ uptake and release rates only slightly altered the bifurcation structures of the model cells. These results suggest that the effect of intracellular Ca2+ dynamics on dynamical properties of SA node pacemaking is relatively small, and that the membrane clock plays a pivotal role in SA node pacemaking. [J Physiol Sci. 2008;58 Suppl:S177]
