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- W1938377867 abstract "We have developed a mathematical model of arterial vasomotion in which irregular rhythmic activity is generated by the nonlinear interaction of intracellular and membrane oscillators that depend on cyclic release of Ca 2+ from internal stores and cyclic influx of extracellular Ca 2+ , respectively. Four key control variables were selected on the basis of the pharmacological characteristics of histamine-induced vasomotion in rabbit ear arteries: Ca 2+ concentration in the cytosol, Ca 2+ concentration in ryanodine-sensitive stores, cell membrane potential, and the open state probability of Ca 2+ -activated K + channels. Although not represented by independent dynamic variables, the model also incorporates Na + /Ca 2+ exchange, the Na + -K + -ATPase, Cl − fluxes, and Ca 2+ efflux via the extrusion ATPase. Simulations reproduce a wide spectrum of experimental observations, including 1) the effects of interventions that modulate the functionality of Ca 2+ stores and membrane ion channels, 2) paradoxes such as the apparently unpredictable dual action of Ca 2+ antagonists and low extracellular Na + concentration, which can abolish vasomotion or promote the appearance of large-amplitude oscillations, and 3) period-doubling, quasiperiodic, and intermittent routes to chaos. Nonlinearity is essential to explain these diverse patterns of experimental vascular response." @default.
- W1938377867 created "2016-06-24" @default.
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- W1938377867 date "1999-09-01" @default.
- W1938377867 modified "2023-10-06" @default.
- W1938377867 title "Minimal model of arterial chaos generated by coupled intracellular and membrane Ca<sup>2+</sup>oscillators" @default.
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- W1938377867 doi "https://doi.org/10.1152/ajpheart.1999.277.3.h1119" @default.
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