Current models for agonist-activated Ca 2+ entry in nonexcitable cells focus on the
capacitative mechanism where entry is activated as a downstream result of the sustained
depletion of agonist-sensitive stores without any direct requirement for inositol phosphates.
This mechanism has been shown to be important for the sustained Ca 2+ signals seen in a
variety of nonexcitable cells under conditions of maximal stimulation. In contrast, relatively
little attention has been given to Ca 2+ entry under more physiological levels of agonist …