S. O. Karakhim, V. F. Gorchev, P. F. Zhuk, S. O. Kosterin
Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
A mathematical model of intracellular calcium homeostasis in smooth muscle cells has been investigated by computer modelling method. The results of calculations showed that for the plasma membrane calcium pump (PMCA) the limiting rate (VmPM) increasing or the Michaelis constant (KmPM) decreasing result in a lowering of the Ca2+ concentration in cytosol and sarcoplasmic reticulum (SR); the slight VmPM decreasing or KmPM increasing result in fluent cytosolic Ca2+ strengthening due to slow basal influx (SBI) since a massive release of Ca2+ from SR does not occur. The further VmPM decreasing or KmPM increasing stimulate the Ca2+-induced Ca2+ release from SR and the system passes into oscillation mode; when the certain low VmPM or high KmPM level is reached the oscillations of Ca2+ concentration in cytosol are stopped, there is only first oscillation after which a new level of cytosolic Ca2+ concentration is formed fluently: this level is higher than in the initial basal condition (IBC). Sensitivity of myocytes with the lowering of VmPM or increasing KmPM to agonist action is rising but sensitivity of myocytes with increasing VmPM or decreasing KmPM to agonist action is reducing. If the PMCA parameters (VmPM or KmPM) are changed then passive influx of Ca2+ in cytosol from extracellular space remains virtually invariable and it is equal to SBI value during the whole process. Initial rate of PMCA in a new equilibrium condition (NEC) is equal virtually to initial rate in IBC: it allows to calculate a new value VmPM or KmPM from cytosolic Ca2+ concentration in NEC.
Key words: calcium homeostasis, calcium pump, plasma membrane, transmembrane calcium transport, mathematical model, limiting rate, Michaelis constant, intracellular calcium.
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