1. Single acinar cells enzymatically isolated from the rat pancreas were subjected to tight‐seal whole‐cell recordings. Changes in cell membrane capacitance and conductance were simultaneously recorded using a phase‐sensitive detection method. 2. Acetylcholine (ACh, 0.05‐0.5 microM) and cholecystokinin octapeptide (CCK‐8, 10‐50 pM) concomitantly induced transient increases in cell membrane current, capacitance and conductance only when cytosolic Ca2+ was weakly chelated by EGTA (70 microM). These responses were prolonged when the cells were dialysed with a solution containing GTP gamma S (a stable analogue of GTP, 50‐100 microM), whereas they were inhibited by dialysing with that containing GDP beta S (a stable analogue of GDP). These results suggest that a type of guanine‐nucleotide‐binding protein (G‐protein) could be involved in ACh‐ or CCK‐receptor signalling. 3. The ACh‐ or CCK‐induced responses (with or without GTP gamma S in the cytosol) were all abolished when a high dose of EGTA (1‐2 mM) was injected into the acinar cells. In addition, A23187, a calcium ionophore, induced sustained responses when the cytosolic Ca2+ was weakly buffered by 70 microM‐EGTA. These results suggest that the secretagogues regulate the changes in cell membrane capacitance and conductance via an increase and decrease of cytosolic Ca2+ concentration. 4. Oscillatory changes in cell membrane conductance and capacitance were consistently observed even without applying secretagogues when the cells were dialysed with a solution containing GTP gamma S (50‐100 microM) and cytosolic free Ca2+ ions weakly buffered at about 10(‐6) M with a low dose of EGTA and CaCl2. 5. The peak amplitude of changes in cell membrane capacitance induced by ACh or CCK‐8, with or without GTP gamma S in the cytosol, varied between 200 and 1000 fF, thereby suggesting that 20‐100 zymogen granules can fuse with the luminal cell membrane in response to these agonists in rat exocrine pancreatic acinar cells.
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