The cholecystokinin-induced increase in intracellular calcium in AR42J cells is mediated by CCKB receptors linked to internal calcium stores

Abstract

Changes in intracellular levels of free [Ca2+]i were monitored in cell suspensions and either single cells or cell clusters of the rat pancreatic tumour cell line AR42J grown on cover slips. Increases in free [Ca2+]i were seen when the bathing medium contained cholecystokinin octapeptide sulphated (CCK) or CCKB receptor agonists. Responses to CCK agonists were repeatable and reversed on washout. The responses to cholecystokinin and pentagastrin could be blocked by selective CCKB receptor antagonists but not a CCKA receptor antagonist. Depleting internal Ca2+ stores with thapsigargin blocked the response to pentagastrin suggesting that the response was mediated by Ca2+ release from internal stores. The rapid run down of the pentagastrin response in the absence of extracellular Ca2+ shows that replenishment of internal stores by extracellular Ca2+ is important in maintaining the CCK response.