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  • 1
    Electronic Resource
    Electronic Resource
    Parotid acinar cells: ionic dependence of acetylcholine-evoked membrane potential changes (1978)
    Springer
    Pflügers Archiv 376 (1978), S. 159-167 
    Details
    ISSN: 1432-2013
    Keywords: Parotid ; Acetylcholine ; Null potential ; Intercellular coupling ; Electrogenic Na pump
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Segments of mouse parotid were placed in a superfusion chamber. Surface acini were impaled by one or two micro-electrodes for measurement of membrane potential and resistance. The acinus under investigation was stimulated by micro-iontophoretic application of acetylcholine (ACh) or adrenaline. Neighbouring acinar cells were electrically coupled. Electrical coupling between acinar cells only occurred within restricted domains probably corresponding to an acinus or a group of acini. Passing direct current through one intracellular electrode, the resting potential of an acinus could be set at desired levels and the dependency of the ACh-evoked potential change on the resting potential investigated. The ACh null potential (initial effect) was about −60mV. A delayed hyperpolarizing effect of ACh could not be reversed. The initial ACh-evoked potential change was sensitive to alterations in extracellular Na, K and Cl concentration. The delayed ACh-evoked hyperpolarization was blocked by ouabain, exposure to Na-free or K-free solutions. It is concluded that ACh increases mainly K and Na membrane conductance causing K efflux and Na influx with a subsequent Na activation of an electrogenic Na pump.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00581579
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The relationship between stimulation-induced potassium release and amylase secretion in the mouse parotid (1977)
    Springer
    Pflügers Archiv 369 (1977), S. 207-211 
    Details
    ISSN: 1432-2013
    Keywords: Parotid ; Amylase secretion ; Potassium release ; α- and β-Adrenoceptor ; Acetylcholine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The output of amylase from superfused mouse parotid segments in response to stimulation with acetylcholine (ACh), phenylephrine and isoprenaline during exposure to solutions with varying potassium concentrations was monitored by an on line automated fluorometric method. 2. During stimulation with ACh or phenylephrine a 10-fold increase in superfusion fluid potassium concentration caused an immediate very marked reduction in amylase output which was fully reversible. A 10-fold reduction in potassium concentration resulted in a prominent rise in amylase output. During stimulation with isoprenaline there was no effect on the amylase output of varying the extracellular potassium concentration. Acetylcholine and phenylephrine caused potassium release from the mouse parotid whereas isoprenaline had no such effect. 3. It appears that under conditions where stimulation-induced potassium release is enhanced there is also an enhanced amylase secretion and vice versa. There may therefore be a link between passive potassium transport and amylase secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00582186
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Separate activation sites for cholecystokinin and bombesin on pancreatic acini (1979)
    Springer
    Pflügers Archiv 382 (1979), S. 263-267 
    Details
    ISSN: 1432-2013
    Keywords: Pancreatic acinar cells ; N2, O2′ dibutyryl guanosine 3′:5′-Monophosphate ; Cholecystokinin antagonist ; Bombesin ; Membrane potential
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of dibutyryl cyclic guanosine 3′:5′ monophosphate (dbcGMP) on the electrical responses of in vitro mouse pancreatic acinar cells to caerulein, bombesin and acetylcholine, applied by microionophoresis, were investigated using intracellular microelectrode recordings. Exposure to dbcGMP (10−3 mol ·l−1) quickly abolished the depolarization response to caerulein ionophoresis, while the bombesin-nonapeptide and acetylcholine-induced depolarizations were retained. Exposing acinar cells to 2×10−4 mol·l−1 dbcGMP reduced their sensitivity such that a 10-fold increase in the applied caerulein ionophoresis current was required to restore the responses to the same magnitude as those obtained in a dbcGMP-free environment. The response to topical applications of pentagastrin and CCK-33 were also abolished by dbcGMP. The results provide direct evidence that functional ACh, bombesin and CCK receptors are all present within the same acinar cell unit. The dbcGMP-induced inhibition of responses evoked by CCK-like peptides is immediate, specific and easily reversible. DbcGMP acts as a competitive antagonist of the CCK receptor on pancreatic acinar cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00583711
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    The role of calcium in parotid amylase secretion evoked by excitation of cholinergic, α- andβ-adrenergic receptors (1977)
    Springer
    Pflügers Archiv 372 (1977), S. 231-237 
    Details
    ISSN: 1432-2013
    Keywords: Parotid ; Amylase secretion ; Calcium ; Manganese ; α- and β-Adrenoceptor ; Acetylcholine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The output of amylase from superfused mouse parotid segments was monitored by an on-line automated fluorometric method. 2. 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. 3. 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. 4. 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. 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. 6. 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. 7. 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+.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01063857
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    Paper (German National Licenses)
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