A mathematical model of the calcium transient in urinary bladder smooth muscle cells.

Abstract

An increase in cytoplasmic calcium (Ca(2+)) concentration ([Ca(2+)]i) is a prerequisite for the contraction of detrusor smooth muscle (DSM) cells . The increase in [Ca(2+)]i is accomplished by Ca(2+) entry mainly via voltage dependent L-type Ca(2+) channel and Ca(2+) release from intracellular stores. We report here a simulation of the processes that regulate intracellular Ca(2+) and their dependence on Ca(2+) concentration. Based on experimentally recorded data, mathematical equations for Ca(2+) current (generated mainly by L-type Ca(2+) channel) are developed along with representation of Ca(2+)ATPase pump currents. The plasma membrane Ca(2+)ATPase (PMCA) pump and sarco/endoplasmic reticulum Ca(2+)ATPase (SERCA) pump are responsible for lowering [Ca(2+)]i which leads to relaxation of smooth muscle. Our model simulates Ca(2+) current, action potential and the Ca(2+) transient response so as to reasonably mimic the experimental recordings. In novel findings, currents produced by PMCA and SERCA along with their amplitude and waveform pattern under voltage clamp condition have been predicted for DSM cells. The model has further been used to produce the Ca(2+) transient which results because of L-type Ca(2+) channel, Ca(2+) release from intracellular store, PMCA, SERCA and presence of buffer in the cytoplasm. To explore the model further, Ca(2+) transient decay rate in control condition is compared to the decay rate reached when PMCA and SERCA are inhibited. We conclude that this model can be used to describe the Ca(2+) transient response produced by the DSM cell in response to depolarization of cell membrane.