Wong A Y, Klassen G A
Department of Physiology and Biophysics, Dalhousie University, Halifax, Canada.
Cell Calcium. 1993 Mar;14(3):227-43. doi: 10.1016/0143-4160(93)90070-m.
A model of smooth muscle cell is proposed to describe the mechanisms by which intracellular calcium (Cai) is regulated when the cell is stimulated by noradrenaline (NA)/agonist (Ag) or depolarized. The intracellular Ca2+ store is comprised of two calcium pools: A-store which is sensitive to inositol 1,4,5 trisphosphate (IP3) and C-store, insensitive to IP3 but sensitive to Cai. The A-store is refilled by Ca2+ from C-store and reuptake of Cai. The uptake rate is dependent on the degree of filling in the A-store. The C-store, activated by Cai, is replenished by extracellular Ca2+ (Cao). IP3 generated by NA or Ag changes the A-store permeability, discharging its Ca2+ into the cytosol. Depolarization activates Ca2+ current through the L-type channels. The following events are simulated and compared with experimental observations: (a) Cai transient stimulated by high K+; (b) Cai transient and Ca2+ efflux induced by shortlasting and longlasting NA in the absence of Cao; (c) effect of lanthanum on NA-induced Cai and Ca2+ efflux; and (d) effects of nifedipine, ryanodine, BAY K 8644 and cyclopiazonic acid on Cai.
