The output of amylase from superfused mouse parotid segments was monitored by an on-line automated fluorometric method.
During exposure to Ca2+-free solution, containing the Ca2+-chelating agent EGTA, excitation of α-adrenoceptors or cholinergic receptors only resulted in a very small and transient increase in amylase output. Admission of Ca2+ during sustained stimulation caused a marked rise in amylase output which was sustained.
During exposure to Ca2+-free solution containing EGTA excitation of β-adrenoceptors caused the usual very marked rise in amylase output and the enhanced amylase secretion was sustained. Admission of Ca2+ during sustained isoprenaline stimulation only caused a small transient rise in amylase output.
The effect of ACh on amylase output varied with the extracellular Ca2+ concentration, being reduced at subnormal extracellular levels and enhanced during superfusion with fluid containing 20 mM Ca2+.
5 mM Mn2+ acted as a stimulant of amylase secretion even in the presence of blocking agents for the cholinergic, α- and β-adrenergic receptor sites. The effect of Mn2+ was biphasic; an initial transient increase in amylase output followed by a slowly developing sustained increase in secretion. The initial response was abolished after pretreatment with EGTA in a Ca2+-free solution.
Adding Mn2+ (5 mM) just after addition of ACh had caused maximal amylase secretion resulted in an immediate reduction in amylase output. Adding Mn2+ and ACh simultaneously to the superfusion solution resulted in a response smaller than that expected for ACh alone. The effect of ACh during continued exposure to Mn2+ (5 mM) was greatly reduced compared to control conditions. Stimulation with Mn2+ during continued exposure to isoprenaline resulted in a marked transient increase in amylase output.
The action of stimulants exciting cholinergic and α-adrenergic receptors is entirely dependent on extracellular Ca2+ whereas the action of stimulants exciting adrenergic β-receptors is relatively independent of Ca2+. Mn2+ immediately inhibits ACh-evoked amylase secretion probably by reducing Ca2+-influx. Mn2+ is, however also a stimulant of amylase secretion probably acting by displacing membrane-bound cell Ca2+.
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Petersen, O.H., Ueda, N., Hall, R.A. et al. The role of calcium in parotid amylase secretion evoked by excitation of cholinergic, α- andβ-adrenergic receptors. Pflugers Arch. 372, 231–237 (1977). https://doi.org/10.1007/BF01063857
- Amylase secretion
- α- and β-Adrenoceptor