The effects of oxymetazoline on secretion of protein and some electrolytes by rat submandibular and parotid glands

Oxymetazoline is a potent secretagogue for the salivary glands of rats. In the parotid gland, it activates preferentially alpha-adrenoceptors. As for the submandibular glands, it activates alpha-adrenoceptors at relatively low doses but at higher doses it allows secretion of new types of proteins.     

The effect of carbonic anhydrase inhibitors on secretion by the parotid and mandibular glands of red kangaroos Macropus rufus

Summary The effects of carbonic anhydrase inhibitors on secretion by macropodine parotid and mandibular glands were investigated using anaesthetized red kangaroos. In the parotid gland, acetazolamide (500 mol·l^-1) reduced a stable acetylcholine-evoked, half-maximal flow rate of 2.02±0.034 to 0.27±0.023 ml·min^-1 (87% reduction). Concurrently, salivary bicarbonate concentration and secretion fell (129.4±1.46 to 80.9±1.63 mmol·l^-1 and 264.8±7.96 to 22.3±2.30 mol·min^-1, respectively), phosphate and chloride concentrations rose (14.0±0.79 to 27.6±0.85 mmol·l^-1 and 5.6±0.25 to 27.5±1.32 mmol·l^-1, respectively), sodium concentration and osmolality were unaltered, and potassium concentration fell (8.8±0.33 to 6.4±0.29 mmol·l^-1). High-rate cholinergic stimulation during acetazolamide blockade was unable to increase salivary flow beyond 11±0.9% of that for equivalent unblocked control stimulation. However, superimposition of isoprenaline infusion on the acetylcholine stimulation caused a three-fold increase in the blocked flow rate. These treatments were accompanied by small increases in salivary phosphate and chloride concentrations but not bicarbonate concentration. Methazolamide infusion caused similar changes in parotid secretion. In the mandibular gland, acetazolamide infusion had no effect on salivary flow rate during either low- or high-level acetylcholine stimulation. Acetazolamide caused no alterrations in salivary electrolyte secretion at low flow rates, but curtailed the rise in bicarbonate concentration associated with high-level acetylcholine stimulation. Acetazolamide administration did not affect the increase in salivary flow rate associated with isoprenaline infusion, but did block the concomitant increase in bicarbonate concentration and secretion substantially. It was concluded that neither cholinergic nor adrenergic stimulation of mandibular fluid secretion depends on secretion of bicarbonate derived from catalysed hydration of CO₂, but a substantial proportion of the increase in bicarbonate secretion during isoprenaline administration, which is probably ductal in origin, is so dependent. In contrast to other salivary glands, including the ovine parotid, fluid secretion by the kangaroo parotid gland during cholinergic stimulation is largely dependent (about 90%) on secretion of bicarbonate derived from hydration of CO₂ catalysed by glandular carbonic anhydrase. Fluid secretion during adrenergic stimulation is not bicarbonate dependent.Abbreviations b.w. body weight - PAH p-aminohippurate - PCO₂ partial pressure carbon dioxide - PCO₂ partial pressure of oxygen     

The noradrenergic innervation of the excretory ducts of the parotid, mandibular and sublingual glands in the rat

Summary The noradrenergic innervation of the excretory ducts of the parotid, mandibular and sublingual salivary glands in the rat has been examined using fluorescence histochemistry. None of the ducts were found to be innervated directly but, in the mandibular duct, innervated blood vessels are in close proximity to the epithelial cells of the duct and it is suggested that noradrenaline may diffuse from the vascular nerve endings to receptors on the epithelial cells.     

Fine structure of the parotid and mandibular glands of the cotton rat (Sigmodon hispidus).

The parotid and mandibular glands of the cotton rat were examined by light and transmission electron microscopy. Parotid gland: Acinar cells were serous in nature, and contained electron-dense granules. Intercalated duct cells contained electron-dense granules. Striated duct cells had small granules of moderate and high electron densities. Mandibular gland: Acinar cells were seromucous in nature, and contained granules of low and moderate electron densities. Intercalated duct cells contained granules of moderate and high electron densities. Striated ducts were comprised of two portions - a secretory portion and a striated portion without granules. The secretory portion had many electron-dense granules. A sexual dimorphism was obserbed in these granules, which were smaller and fewer in females than in males.     

The effects of alpha-methylnoradrenaline on protein and electrolyte secretion by rat submandibular and parotid glands

alpha-Methylnoradrenaline (alpha-mNA) is a potent secretagogue for the parotid and submandibular glands of rats. With regard to the parotid glands, alpha-mNA activates mainly beta-adrenoceptors. In the submandibular glands, alpha-mNA activates alpha-adrenoceptors at higher doses whereas at relatively lower doses it activates beta-adrenoceptors. alpha-mNA may not stimulate the specific alpha 2-adrenoceptors of the salivary glands of rats.     

A comparative study of salivary secretion by parotid and mandibular glands of anaesthetized Capra hircus: effect of pilocarpine

A study was made of basal secretion and the effect of the infusion of pilocarpine on the flow and composition of saliva in the parotid and mandibular glands of the anaesthetized lactating goat. In the parotid gland there was a basal flow (1.6 +/- 0.29 microliter/min) which was not present in the mandibular gland. There is a statistically significant dose-effect relationship between pilocarpine and salivary flow in both glands. Salival composition and its variation with respect to the flow of saliva did not conform to either of the two glands to an exclusive monogastric or ruminant model.     

Inhibitory effect of colchicines on amylase secretion by rat parotid glands: possible localization in the golgi area

Colchicine inhibited amylase secretion by isolated rat parotid glands only 6 h after administration of the drug in vivo. This delayed effect was not the result of the inability of the drug to reach its reaction site. When parotid glands were emptied of their secretory granules by isoproterenol treatment, the subsequent replenishment of cells with granules was inhibited by colchicines. Colchicine concomitantly produced alterations of the Golgi complexes, the cisternae of which were reduced in size and surrounded by clusters of microvesicles. Incubation of parotid glands with colchicines for prolonged durations failed to alter stored amylase secretion as stimulated by isoproterenol, but it inhibited the release of de novo synthesized enzyme. Another colchicines-binding activity, firmly bound to the particular fraction of homogenates, was found, of which a part may represent membrane located microtubular protein. An assembly-disassembly cycle of microtubules appears to exist in the parotid gland, as in the liver. However, only 14 percent of tubulin was found to be polymerized as microtubules in parotid glands as opposed to 40 percent in the liver. The present data suggest that colchicine primarily inhibits the transfer of secretory material towards or away from the Golgi complexes but not the hormone-stimulated secretion of stored amylase.     

In vivo effects of tunicamycin on the secretory processes of rat parotid glands

Summary The morphological and functional effects of tunicamycin were studied in rat parotid glands at the stage of the reformation of secretory granules following secretory stimulation by isoproterenol. Tunicamycin inhibited the incorporation of (³H)-mannose into the acid-insoluble fraction but had no effect on total protein synthesis as determined by the incorporation of (¹⁴C)-leucine. Thus the administration of tunicamycin in vivo inhibits the synthesis of mannose-rich glycoproteins in a manner similar to that in an in vitro system. The ultrastructure of the acinar cell showed little change following treatment with this drug, except that the number of reaccumulated secretory granules was greater than in the control. Amylase secretion stimulated by isoproterenol was inhibited in tunicamycin-treated cells, but did not decrease following treatment with N⁶,2-O-dibutyryladenosine 3-5-cyclic monophosphate, a secretory stimulator bypassing the -receptor. A radio-receptor assay using (³H)-dihydroalprenolol and direct localization using the fluorescent -adrenergic blocker 9-amino-acridin propranolol showed a marked reduction in the binding activity of -receptor following treatment with tunicamycin. Thus the inhibition of N-linked glycosylation appears to produce profound effects on the -adrenergic receptor-adenylate cyclase complex of acinar cells, although the steps of the transport and the exocytotic discharge of secretory materials are not affected.