Fig. 2.

Response of model to application of exogenous noradrenaline and endogenous calcium. (A) $\left[{\mathit{AM}}_P\right]$ response to constant application of $\left[\mathit{NA}\right]$. Simulation data (solid) exhibits a steeper relation than the experimental data (broken lines) of Sjoblom-Widfeldt and Nilsson (1989) for the tensile response of small mesenteric arteries. Experimental data points (±SEM) are conducted in the presence of extracellular calcium concentration 1.0 mM. Note the fitting of the model to the experimental data for high $\left[\mathit{NA}\right]$, which diverges when $\left[\mathit{NA}\right]<1.8\mathrm{\mu }\mathrm{M}$. (B) The force developed by our SMC model as a function of ${[{\mathrm{Ca}}^{2+}]}_{\mathit{SMC}}$. The concentration of actin bound to phosphorylated myosin $\left[{\mathit{AM}}_P\right]$ in the model, followed a sigmoid relationship. Experimental observations from Yagi et al. (1988) show that the $\left[{\mathit{AM}}_P\right]$ closely resembles the force in $\mathrm{\mu }\mathrm{N}$. (C) The response of ${[{\mathrm{Ca}}^{2+}]}_{\mathit{SMC}}$ to exogenous application of $\left[\mathit{NA}\right]=1\mathrm{\mu }\mathrm{M}$ (blue) and $0.1\mathrm{\mu }\mathrm{M}$ (green). The delayed, transient rise, followed by a steady-state plateau fits simulations of Bennett et al. (2005) (dashed), and therefore similarly fits experimental data of Li et al. (1993). These data support our quasi-steady state assumption for the receptor dynamics. (For interpretation of the references to color in this figure caption, the reader is referred to the web version of this article.)