title: Effects of monensin on amylase release from mouse parotid acini.
abstract: Isolated mouse parotid acinar cells (acini) were prepared by enzyme digestion, divalent cation depletion, and mechanical shearing. Acini were found to be morphologically intact, i.e., 95% viable as judged by trypan blue exclusion. Amylase release by the cholinergic agonist carbachol, by the beta-adrenergic agonist isoproterenol, and by monensin was similar to responses obtained in mouse parotid fragments. Monensin-stimulated amylase release was associated with enhanced 22Na+ uptake and 45Ca2+ efflux; monensin did not affect 45Ca2+ uptake. In the absence of extracellular Na+, the response to monensin (50 microM) was reduced from 162 +/- 33.5 to 12.4 +/- 0.5%; monensin also failed to stimulate 45Ca2+ efflux. Similar results were obtained with isoproterenol (10(-6) M). The results suggest that Na+ ions may play a role in amylase release possibly by releasing Ca2+ from internal stores.
mesh_terms: D000681:Amylases / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000502:physiology; D002217:Carbachol / Q000494:pharmacology; D005663:Furans / Q000494:pharmacology*; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D051379:Mice; D008985:Monensin / Q000494:pharmacology*; D010306:Parotid Gland / Q000187:drug effects / Q000201:enzymology*; D012964:Sodium / Q000502:physiology
chemical_list: D005663:Furans; D002217:Carbachol; D008985:Monensin; D012964:Sodium; D000681:Amylases; D007545:Isoproterenol; D002118:Calcium