Pituitary corticotroph cells generate repetitive action potentials and associated Ca2+ transients in response to the agonist corticotropin releasing hormone (CRH). There is indirect evidence suggesting that the agonist, by way of complex intracellular mechanisms, modulates the voltage sensitivity of the L-type a2+ discuss some of the Hodgkin-Huxley type models we have constructed of this process, which have indicated that an increase in the L-type Ca2+ current is sufficient to generate repetitive action potentials. In particular we discuss the effects of including Ca2+ transport between cytosolic and endoplasmic compartments, and the spatial variation in our description of the endoplasmic reticulum (ER) and cytosolic [ Ca2+]. We have found firstly that this [Ca2+] spatial variation did not significantly affect the generation of action potentials, and secondly that a gradual increase in the ER Ca2+ during repetitive action potential activity can ultimately feed back sufficient Ca2+ into the cytosol to eliminate action potentials. We discuss ways in which cells might regulate their intracellular [ Ca2+] dynamics to avoid such an effect. We also investigate the bursting type behaviour inherent in the model.