Cycling of cations between T-tubular and surface membranes in a model of guinea-pig ventricular cardiomyocyte
| Authors | |
|---|---|
| Year of publication | 2005 |
| Type | Article in Periodical |
| Magazine / Source | Journal of Molecular and Cellular Cardiology |
| MU Faculty or unit | |
| Citation | |
| Field | Physiology |
| Keywords | cardiac cell; tubular system; ion cycling; quantitative modelling |
| Description | The contribution of surface and t-tubular membranes to cation homeostasis was evaluated in a model of the guinea-pig ventricular myocyte with a single-compartment representation of the transverse-axial tubular system (TATS) matching detailed ultrastructural data (1), with 53% of the cell membrane in the TATS, and ionic diffusion data (2). The TATS fraction of ion transfer mechanisms was set to 0.53 (uniform distribution) except for INa and ICaL (0.64), IK1 (0.8), Na/Ca exchange (0.7) and Ca-pump (0.2). At steady-state during 4 Hz stimulation in current-clamp, 67% of Ca2+ influx occurred across the TATS membrane, while 53% of Ca2+ extrusion occurred across the surface membrane. Thus the TATS membrane mediates net Ca2+ influx, while the surface membrane mediates net Ca2+ efflux. Transient partial depletion of Ca2+ within the TATS lumen during the action potential was compensated by diffusion from the bulk external solution. Thus within a single beat there was net intracellular Ca2+ flux from the TATS membrane to the surface membrane, and Ca2+ diffusion from the bulk extracellular solution into the TATS completed the cycle to produce steady-state conditions. Similar cycling was computed for Na+, whereas K+ cycled from the surface sarcolemma to the TATS membrane. Thus it appears that the differential localization of ion transfer mechanisms and the depletion of Ca2+ and Na+ (and accumulation of K+) in the TATS lumen result in specialised roles for each membrane, with TATS causing most of the excitation-induced changes of intracellular cation concentrations and the surface membrane being predominantly responsible for their restoration during diastole. |
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