A cytochemical study of the effect of cholinergic and ?-adrenergic stimulation on calcium fluxes of rat parotid gland

1983 ◽  
Vol 79 (2) ◽  
pp. 193-203 ◽  
Author(s):  
H. W. Sampson ◽  
D. J. Kiessel ◽  
L. MacKenzie-Graham ◽  
I. Piscopo
1985 ◽  
Vol 33 (9) ◽  
pp. 942-950 ◽  
Author(s):  
M R Mazariegos ◽  
A R Hand

Previous studies have shown that tight junctions of the unstimulated rat parotid gland are impermeable to retrogradely administered tracers such as myoglobin. Permeability is increased following beta-adrenergic stimulation, allowing the tracers to reach the intercellular and interstitial spaces. Reaction product of retrogradely infused horseradish peroxidase (HRP) and lactoperoxidase in found in the intercellular and interstitial spaces in both resting and stimulated glands, and many acinar and duct cells contain diffuse cytoplasmic reaction product. In this study we investigate several factors that might influence the distribution of HRP in the parotid gland. Tracer distribution was similar with HRP obtained from different suppliers, with different HRP preparations (Sigma types II, VI, VIII, and IX), and at HRP concentrations of 0.1-10 mg/ml. Inclusion of various saccharides in the infusion solution had no effect on the distribution of reaction product. Inhibition of the enzymatic activity of HRP by extraction of the heme group or reaction with hydrazine reduced but did not eliminate the extraluminal and cytoplasmic reaction product. In contrast, HRP treated with high H2O2 concentrations (0.04 M) was retained in the lumina and cytoplasmic staining was nearly abolished. Immunofluorescent localization of untreated and H2O2-treated HRP after retrograde infusion confirmed the findings obtained using diaminobenzidine procedures. These results suggest that the peroxidatic activity of HRP may damage cell membranes and tight junctions in the rat parotid gland, and indicate that permeability studies employing HRP as a tracer should be interpreted with caution.


1987 ◽  
Vol 66 (2) ◽  
pp. 552-556 ◽  
Author(s):  
E.E. Kousvelari ◽  
P.C. Fox ◽  
B.J. Baum

Activation of β-adrenoreceptors in rat parotid acinar cells leads to copious exocrine protein secretion. Additionally, β-adrenergic stimulation dramatically increases specific secretory protein synthesis and enhances N-linked glycosylation of secretory glycoproteins. Recently, efforts have been directed toward understanding the mechanisms underlying these biosynthetic events. We have been particularly interested in the receptor-mediated regulation of glycosylation. In this report, we evaluate available mechanistic information from the rat parotid gland and present initial data examining the ability of various regulatory agents to modulate N-linked glycosylation in enzymatically-dispersed cell aggregates from surgical specimens of human parotid glands. We conclude that glycosylation of human parotid N-linked glycoproteins may be regulated by extracellular signaling similar to that operative in the rat parotid gland.


1974 ◽  
Vol 138 (1) ◽  
pp. 47-52 ◽  
Author(s):  
Robert H. Michell ◽  
Lynne M. Jones

1. Adrenergic agonists provoke a marked increase in labelling of phosphatidylinositol in fragments of rat parotid gland. 2. Adrenaline and phenylephrine (an adrenergic α-agonist) are effective stimulants, but isoprenaline (an adrenergic β-agonist) is relatively ineffective. 3. The response evoked by phenylephrine or adrenaline is prevented by prior incubation of the tissue with phenoxybenzamine (an α-receptor blocking agent), but not by prior incubation with pindolol (a β-receptor blocking agent). 4. Adrenergic stimulation of phosphatidylinositol metabolism in parotid gland is therefore mediated through α-receptors, in common with the adrenaline-induced K+ efflux. It is not linked to enzyme secretion, which is triggered by stimulation of β-receptors. 5. It is suggested that the stimulation of phospholipid metabolism that occurs in several other tissues in the presence of adrenaline or noradrenaline may also involve α-receptors.


1971 ◽  
Vol 246 (12) ◽  
pp. 3879-3884 ◽  
Author(s):  
Leo M. Sreebny ◽  
Dorthea A. Johnson ◽  
Murray R. Robinovitch

1996 ◽  
Vol 155 (3) ◽  
pp. 172-183 ◽  
Author(s):  
D. Ježek ◽  
L. Banek ◽  
T. Banek

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