Fig. 9.

Relative contribution of late Na⁺ current to changes in atrial myocyte ion homeostasis and Ca²⁺/calmodulin-dependent protein kinase (CaMKII) signaling. Regression coefficients showed how changes in the model parameters affected ion homeostasis and CaMKII activity in baseline wild-type (WT) simulated cells (A–D) and in the presence of the β-adrenergic agonist isoproterenol (E–H). Shown are parameter sensitivities of ion channel conductance parameters affecting maximum diastolic intracellular Na⁺ concentration ([Na⁺]_i; A and E), maximum intracellular Ca²⁺ concentration ([Ca²⁺]_i; B and F), maximum Ca²⁺ concentration in the sarcoplasmic reticulum ([Ca²⁺]_SR; C and G), and maximum fraction of activated CaMKII subunits (D and H). Abbreviations are as follows: gTo, maximal conductance (gMax) of the transient outward K⁺ current; gK1, gMax of the inward rectifier K⁺ current; gKr, gMax of the rapid delayed rectifier K⁺ current; gKs, gMax of the slow delayed rectifier K⁺ current; gKur, gMax of the ultrarapid K⁺ current; gNa, gMax of the rapid Na⁺ current; gNaca, maximal transport rate of the Na⁺/Ca²⁺ exchanger; gNaL, gMax of the late Na⁺ current; JSRrel, maximal Ca²⁺ release flux from the junctional sarcoplasmic reticulum; JSRup, maximal Ca²⁺ uptake rate into the sarcoplasmic reticulum; gCaL, gMax of the L-type Ca²⁺ channel.