1992
DOI: 10.1016/0003-9969(92)90109-l
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Differential regulation of agonist-stimulated Ca2+ influx in acini of rat pancreas and submandibular gland

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Cited by 6 publications
(2 citation statements)
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“…Rat submaxillary gland has frequently been studied for pharmacological characterization of the MChRs involved in secretion by examining the following assays: 86 rubidium efflux ( Bovell et al ., 1989 ), calcium mobilization ( Hurley & Brinck, 1992 ; Valdez & Turner, 1991 ), inositol phosphates accumulation ( Laniyonu et al ., 1990 ; Abdallah et al ., 1992 ), and inhibition of adenylyl cyclase activity ( Dai et al ., 1991 ; Laniyonu et al ., 1990 ; Abdallah et al ., 1992 ). While these approaches offer some insight into cellular function in rat submaxillary gland, they generally lack a robust method to determine antagonist affinity and thus characterize the muscarinic subtype.…”
Section: Introductionmentioning
confidence: 99%
“…Rat submaxillary gland has frequently been studied for pharmacological characterization of the MChRs involved in secretion by examining the following assays: 86 rubidium efflux ( Bovell et al ., 1989 ), calcium mobilization ( Hurley & Brinck, 1992 ; Valdez & Turner, 1991 ), inositol phosphates accumulation ( Laniyonu et al ., 1990 ; Abdallah et al ., 1992 ), and inhibition of adenylyl cyclase activity ( Dai et al ., 1991 ; Laniyonu et al ., 1990 ; Abdallah et al ., 1992 ). While these approaches offer some insight into cellular function in rat submaxillary gland, they generally lack a robust method to determine antagonist affinity and thus characterize the muscarinic subtype.…”
Section: Introductionmentioning
confidence: 99%
“…The reason for the difference in the Cl and K changes seen after cholinergic and α-adrenergic stimulation cannot be ascertained from the results of this study, but may be related to differences in the extent to which each type of agonist activates intracellular signals regulating ion channels and fluxes. Both Cland K + efflux from salivary cells occur through channels regulated by the level of free cytosolic Ca 2+ (Martinez and Cassity 1986;Martinez and Camden 1989;Martinez 1990) and preliminary evidence indicates that α-adrenergic stimuli cause a smaller increase in cytosolic Ca 2+ than cholinergic stimuli (Hurley and Brinck 1992;Puente et al 1996;Willis et al 1996). This difference in Ca 2+ -mediated signalling could explain the smaller volume of secretion produced by α-adrenergic agonists.…”
Section: Discussionmentioning
confidence: 99%