Ca²⁺ Dynamics in Rat Pancreatic AR-42J and AR-IP Cells

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Spatiotemporal change of the cytosolic free Ca²⁺ concentration ([Ca²⁺]_i) in response to a variety of secretagogues was examined in rat pancreatoma AR-42J and AR-IP cells by microspectroflurometry and digital imaging microscopy after loading with fura-2. In the presence of external Ca²⁺, carbachol, CCK-OP (cholecystokinin-octapeptide), gastrin, norepinephrine or high K⁺ evoked a large transient increase in [Ca²⁺]_i in AR-42J cells which declined to a sustained level before slowly declining towards the resting level. In the absence of external Ca²⁺, a transient increase in [Ca²⁺]_i were evoked by all the ligands except for high K⁺ stimulation, which declined rapidly towards the resting level. The [Ca²⁺]_i increase caused by carbachol and high K⁺ treatment was inhibited by muscarinic receptor antagonist, atropin, and by L-type Ca²⁺ channel blocker, nifedipin, respectively. The transient [Ca²⁺]_i increase induced by gastrin stimulation was not blocked by Ca²⁺ channel blocker, lanthanum. In the AR-IP cells, which are non-differentiated pancreatoma cell line, all stimulations including high K⁺ treatment have failed to evoke [Ca²⁺]_i response. These intracelluar Ca²⁺ mobilizations in response to ligands in AR-42J cells were displayed by digital imaging microscopy. From these results we conclude that AR-42Jcells has an α-adrenergic receptor, in addition to muscarnic acetylcholine receptor, CCK-OP receptor, gastrin receptor and voltage dependent Ca²⁺ channel. In marked contrast, AR-IP cells have neither any hormonereceptor for the above ligands nor voltage dependent Ca²⁺channel.