Secretion Of Parotid Saliva Research Articles

Parotid hypersalivation after inferior salivatory nucleus glutamate/NMDA receptor excitation in the rat

Although salivation is essential during eating behavior, little is known about the brainstem centers that directly control the salivary glands. With regard to the inferior salivatory nucleus (ISN), the site of origin of the parasympathetic preganglionic cell bodies that innervate the parotid glands, previous anatomical studies have located it within the rostrodorsal medullary reticular formation. However, to date there is no functional data that shows the secretory nature of the somas grouped in this region. To activate only the somas and rule out the activation of the efferent fibers from and the afferent fibers to the ISN, in exp. 1, NMDA neurotoxin was administered to the rostrodorsal medullary region and the secretion of saliva was recorded during the following hour. Results showed an increased secretion of parotid saliva but a total absence of submandibular-sublingual secretion. In exp. 2, results showed that the hypersecretion of parotid saliva after NMDA microinjection was completely blocked by the administration of atropine (a cholinergic blocker) but not after administration of dihydroergotamine plus propranolol (α and β-adrenergic blockers, respectively). These findings suggest that the somata of the rostrodorsal medulla are secretory in nature, controlling parotid secretion via a cholinergic pathway. The data thus functionally supports the idea that these cells constitute the ISN.

Effects of Isoflurane Anesthesia and Pilocarpine on Rat Parotid Saliva Flow

The purpose of this study was to investigate the effects of isoflurane on unstimulated and pilocarpine-stimulated parotid saliva secretion. Ten male Sprague-Dawley rats weighing 350-400 g were randomized into two groups, and the saliva flow rate and lag phase were measured at two doses of isoflurane in a crossover study design. Increasing the isoflurane concentration from 1% to 2% was associated with a 19% decrease in saliva secretion rate, and the lag to saliva secretion was increased by 155%. To clarify whether the effect of isoflurane (1.5%) on the parotid flow varied with stimulus intensity, we measured the parotid flow induced by seven different doses of pilocarpine on sham-irradiated rats and rats irradiated with single doses of 15 Gy. A maximal pilocarpine response was obtained with 1.5 mg/kg in both irradiated and sham-irradiated rats; however, the parotid flow of the irradiated rats was 50% slower than that of the sham-irradiated rats. In conclusion, 1.5% isoflurane was found to be a good compromise between proper anesthesia and isoflurane-induced inhibition of saliva secretion. Pilocarpine induces saliva secretion in a dose-dependent matter, with supra-maximal stimulation achieved using 1.5 mg/kg.

Nicotinic receptor agonist-induced salivation and its cellular mechanism in parotid acini of rats

Cigarette smoking and nicotine enhance parotid saliva secretion, however, the underlying mechanism is unclear. To address the mechanism of nicotine-induced salivation and to explore the possibility that nicotinic receptor agonists act as sialogogues, we investigated the effects of nicotinic receptor agonists on salivary secretion in vivo and on intracellular Ca 2+ concentration in digested parotid acini in vitro in rats. In urethane-anesthetized rats, intravenous administration of nicotinic receptor agonists, nicotine and cytisine, at 3 μmol/kg increased whole saliva output accompanied by a pressor response with nicotine, but not with cytisine. Using Ca 2+-imaging system on digested parotid acini in which autonomic nerve terminals were kept intact, nicotine and cytisine dose-dependently increased intracellular Ca 2+ concentration at μM level. This was not observed in single acinar cells containing no nerve terminal. The nicotine-induced Ca 2+ response was largely blocked by a muscarinic receptor antagonist and partly blocked by an adrenergic receptor antagonist. Furthermore, the same nicotine-induced Ca 2+ response was blocked by mecamylamine, a relatively selective nicotinic antagonist for α3β4 subtype receptor, but not by other selective antagonists, dihydro-β-erythroidine for α4-containing receptor and methyllycaconitine for α7 nicotinic receptors. These results suggest that nicotinic agonists-induced salivation is due to a release of acetylcholine and noradrenaline from autonomic nerve terminals through activation of α3β4 nicotinic receptor subtype. In addition, considering the blood pressure response and development of addiction with nicotine, cytisine may be a better therapeutic candidate to serve as a sialogogue for xerostomia patients.

Parotid salivary secretion induced by stimulation of periodontal regions with toothbrush in humans

The act of brushing teeth induces salivary secretion. However, there is no evidence to show which particular regions of the teeth and oral cavity in brushing induces the most effective salivary secretion. We investigated the effects of tooth brushing in different oral regions on parotid salivary secretion in humans. Saliva was collected using a modified Lashley cup. Brushing of the gingival margin was performed according to the Bass method, which may stimulate periodontal mechanoreceptors. The occlusal surface of the molars, gingiva, tongue, and palatal rugae were also brushed with a toothbrush. Compared to the flow rate of saliva from the unstimulated parotid gland, the salivary flow rates were enhanced when every oral region was brushed. The flow rate produced by brushing the palatal gingival margin of the ipsilateral maxillary molars was greater than that produced by brushing the occlusal surface of ipsilateral maxillary molars and palatal gingiva beside the molars. The flow was also significantly greater than that produced by brushing the palatal gingival margins of the contralateral maxillary molars, the maxillary/mandibular incisors, the dorsum of tongue and the palatal rugae. No significant difference was observed between brushing the gingival margins of the ipsilateral maxillary versus mandibular molars. These data indicate that brushing the gingival margin of molars is the most effective region to stimulate parotid saliva secretion. This likely activates periodontal mechanoreceptors, and this technique may be a simple way to improve salivary secretion in oral rehabilitation. The degree of salivary secretion caused by brushing the teeth is specific to particular oral regions. Brushing of the gingival margins is the most effective location to induce parotid salivary secretion.

Mechanisms Controlling Feed Intake in Large-type Goats Fed on Dry Forage

An intracerebroventricular (ICV) infusion of somatostatin 1-28 (SRIF) was used as a thirst-controlling peptide antagonist to investigate whether or not thirst-controlling peptides are involved in the significant decrease in feed intake during the initial stages of feeding large-type goats on dry forage. A continuous ICV infusion of SRIF was conducted at a small dose of 4 μg/0.2 ml/h for 27 h from day 1 to day 2. Goats (n 5) were fed roughly crushed alfalfa hay cubes for 2 h twice daily and water was given ad libitum. Feed intake was measured during ICV infusion of artificial cerebrospinal fluid (ACSF) and SRIF. The feed intake during SRIF infusion increased significantly compared to that during ACSF infusion. In comparison to the ACSF treatment, plasma osmolality during the SRIF treatment significantly decreased during the first half of the 2 h feeding period. The factor causing the decrease in plasma osmolality during the ICV infusion of SRIF was a decrease in plasma Na, K, Cl, and Mg concentrations. In comparison to the ACSF infusion treatment, parotid saliva secretion volumes during the 2 h feeding period in the SRIF infusion treatment were significantly larger. While there was no significant difference in cumulative water intake (thirst levels) between the SRIF and the ACSF treatments upon conclusion of the 2 h feeding period, based on the plasma osmolality results it is thought that thirst level increases brought about by alfalfa hay cube feeding in the first half of the feeding period were reduced. It is thought that the somatostatin-induced increases in feed intake during the 2 h feeding period in the present experiment were caused by decreases in plasma osmolality brought about by the somatostatin infusion. As a result, it is suggested that the significant decrease in feed intake during the initial stages of feeding in large-type goats given roughly crushed alfalfa hay cubes, was due to the actions of thirst-controlling peptides.

Physiological Factors Depressing Feed Intake and Saliva Secretion in Goats Fed on Dry Forage

Ruminants eating dry forage secrete large volumes of saliva which results in decreased plasma volume (hypovolemia) and the loss of NaHCO 3 from the blood. The present research investigated whether or not hypovolemia and the loss of NaHCO 3 from the blood in goats brought about by dry forage feeding actually depresses feed intake and saliva secretion, respectively. The present experiment consisted of three treatments (NI, ASI, MI). In the control treatment (NI), a solution was not infused. In the ASI treatment, i.v. infusion of artificial parotid saliva was initiated 1 h before feeding and continued for the entire 2 h feeding period. In the MI treatment, iso-osmotic mannitol solution was infused. The NI treatment showed that hematocrit and plasma total protein concentration were increased due to decreased circulating plasma volume brought about by feeding. In the ASI treatment, the fluid and NaMCO 3 that were lost from the blood because of a feeding-induced acceleration of saliva secretion was replenished with an intravenous infusion of artificial parotid saliva. This replenishment lessened the levels of suppression on both feeding and parotid saliva secretion. When only the lost fluid was replenished with an intravenous infusion of iso-osmotic mannitol solution in the MI treatment, the degree of feeding suppression was lessened but the level of saliva secretion suppression was not affected. These results indicate that the marked suppression of feed intake during the initial stages of dry forage feeding was caused by a feeding-induced hypovolemia while the suppression of saliva secretion was brought about by the loss of NaHCO 3 from the blood due to increased saliva secretion during the initial stages of feeding.

Controlling Factors of Feed Intake and Salivary Secretion in Goats Fed on Dry Forage

The purpose of this research was to determine whether or not feeding induced hypovolemia (decreases in plasma volume) and decreases in plasma bicarbonate concentration caused by loss of NaMCO 3 from the blood, act to suppress feed intake and saliva secretion volumes during the initial stages of feeding in goats fed on dry forage. The animals were fed twice a day at 10:30 and at 16:00 for 2 h each time. Prior to the morning feeding, the collected saliva (3-5 kg) was infused into the rumen. During the morning 2 h feeding period (10:30 to 12:30), the animals were fed 2-3 kg of roughly crushed alfalfa hay cubes. At 16:00, the animals were fed again with 0.8 kg of alfalfa hay cubes, 200 g of commercial ground concentrate and 20 g of sodium bicarbonate. In order to compensate for water or NaHCO 3 lost through saliva during initial stages of feeding, a 3 h intravenous infusion (17-19 ml/min) of artificial mixed saliva (ASI) or mannitol solution (MI) was begun 1 h prior to the morning feeding and continued until the conclusion of the 2 h feeding period. The physiological state of the goats in the present experiment remained unchanged after parotid gland fistulation. Circulating plasma volume decreases caused by feeding (estimated by increases in plasma total protein concentration) were significantly suppressed by the ASI and MI treatments. During the first 1 h of the 2 h feeding period, plasma osmolality in the ASI treatment was the same as the NI (non-infusion control) treatment, while plasma osmolality in the MI treatment was significantly higher. In comparison to the NI treatment, cumulative feed intake levels for the duration of the 2 h feeding period in the ASI and MI treatments increased markedly by 56.6 and 88.3%, respectively. On the other hand, unilateral cumulative parotid saliva secretion volume following the termination of the 2 h feeding period in the ASI treatment was 50.7% higher than that in the NI treatment. MI treatment showed the same level as the NI treatment. The results of the present experiment proved that the humoral factors involved in the suppression of feeding and saliva secretion during the initial stages of feeding in goats fed on dry forage, are feeding induced hypovolemia and decrease in plasma HCO 3 - concentration caused by loss of NaHCO 3 from the blood.

Salivary gland function in persons with ectodermal dysplasias

Ectodermal dysplasias (EDs) constitute a group of conditions comprising developmental defects in two or more of the following tissues: hair, teeth, nails, and sweat glands. The aim of the present study was to contribute to a better understanding of salivary gland involvement in EDs. An ED group (n = 39, median age 12 yr; 24 males, 15 females) and a healthy age- and sex-matched control group were studied. Citric acid stimulated submandibular and parotid salivary flow rates and salivary concentrations, and output of total protein, acidic proline-rich proteins and histatins were analysed. The associations between quantitative and qualitative salivary parameters were also studied. In the ED group, 13 persons (33%) demonstrated a significantly reduced secretion of submandibular and/or parotid saliva, in addition to a low unstimulated and/or chewing-stimulated whole salivary flow. In the ED group as a whole, a reduced median secretory rate of submandibular saliva was found, whereas the median concentrations of some protein parameters were increased. However, the overall output of proteins was normal or reduced. Submandibular glands seemed to be more affected than parotid glands in EDs. In conclusion, salivary secretory tests are recommended in persons with known or suspected EDs.

Effect of Parotid Saliva Secretion on Dry Forage Intake in Goats

Research was carried out to clarify whether a suppression of dry forage intake during the early stages of feeding in ruminants is caused by feeding induced hypovolemia which is produced by the accelerated secretion of parotid saliva. Goats with a parotid fistula were fed roughly crushed alfalfa hay cubes, commercial ground concentrate feed and NaHCO 3 twice daily (10:00-12:00, 16:00-18:00). The animals were free access to drinking water all day prior to, during and after experiments. The animals were intraruminally infused every day prior to the morning feeding period with parotid saliva collected from the parotid fistula over a 24 h period. The present experiment consisted of two treatments, non-infusion (RNI) and intraruminal infusion of parotid saliva (RSF). In the RSF treatment, 4-5 kg of parotid saliva (280-290 mOsm/l) collected over a 24 h period was intraruminally infused 1 h prior to the commencement of the morning feeding. During feeding, eating and parotid saliva secretion rates were measured. Blood samples were also periodically collected from the jugular vein. During and after 2 h feeding, water intakes were measured, respectively. These measurements were used to define thirst levels. It is thought that rumen fill in the RSF treatment was higher than the RNI treatment. Plasma osmolality in the RSF treatment increased in the first half of the 2 h feeding period due to the intraruminal infusion of parotid saliva. Therefore, parotid saliva secretion rates in the RSF treatment were lower than the RNI treatment for 30 min period from 30 to 60 min after the commencement of feeding. On the other hand, plasma total protein concentration and hematocrit in the RSF treatment decreased by 3.2 and 3.3% prior to the commencement of feeding due to the intraruminal infusion of parotid saliva. In the first half of the 2 h feeding period, plasma total protein concentration and hematocrit in the RSF treatment showed a tendency to decrease compared to the RNI treatment. Thirst level in the RSF treatment during feeding was approximately 31.3% less than the RNI treatment. Upon the completion of the 2 h feeding period, cumulative feed intake in the RSF treatment was significantly larger (19.7%) than the RNI treatment. The results suggest that a suppression of dry forage intake during the early stages of feeding in goats is partly caused by feeding induced hypovolemia, which is produced by the accelerated secretion of parotid saliva.

High beta-galactosidase and ganglioside GM1 levels in the human parotid gland.

Ganglioside G(M1) is a membrane glycolipid typical of nerve cell membranes, where it partakes in neurotransmitter release and is catabolized by the lysosomal beta-galactosidase (GM1ase) (EC 3.2.1.23). After demonstrating a novel degenerative disease of the parotid gland in mice deficient in GM1ase, mimicking the human storage disease GM(1) gangliosidosis, we studied GM1ase and ganglioside G(M1) content in the human parotid glands. Levels of GM1ase and ganglioside G(M1) were determined in samples of parotid tissues and neighboring muscle (as a negative control) for 3 subjects. Tissues were also processed for histochemical demonstration of GM1ase. The mean specific activity of GM1ase was more than 6-fold higher in the healthy human parotid tissues (1.4 +/- 0.5 nmol of 4-methylumbelliferone per minute per milligram of protein) relative to the neighboring muscle tissue (0.23 +/- 0.07 nmol of 4-methylumbelliferone per minute per milligram of protein). Activity of GM1ase was histochemically localized mainly to striated duct and acinar cells of the parotid gland. Ganglioside G(M1) content in the parotid gland was on average 30-fold higher relative to muscle. Our results are consistent with previous findings reported in the mouse and the rabbit, and probably reflect a general property of the mammalian parotid glands. The novel mechanism we previously proposed for the mouse parotid saliva secretion, mimicking neurotransmitter release in ganglioside G(M1)-containing nerve cells, is probably applicable also to the human parotid gland. Similarly, the human parotid gland is probably also severely affected in GM(1) gangliosidosis.

The secretion of parotid saliva as stimulated by 10% citric acid is not related to precipitating factors in burning mouth syndrome.

Burning mouth syndrome (BMS) is known to have multiple precipitating factors and exists in various clinical subtypes. If salivary gland function was compromised in BMS it could help explain the link with diverse precipitating factors. This study quantified stimulated right and left parotid flow rates (SPFR) in 114 patients with BMS. It also attempted to correlate SPFR with haematinic parameters, oral candidal carriage, concurrent drug therapy and BMS subtype. No relationship was found between haematinic parameters and SPFR nor between SPFR and oral candidal carriage. Patients with Type 2 BMS had a significant reduction in SPFR. Antidepressant medication was associated with reduced SPFR but there was no such association with either tranquillisers or hypnotics. These results provide evidence of reduced parotid gland function in Type 2 BMS and a role for antidepressant medication in reducing SPFR.

Effect of donor age on the concentrations of histatins in human parotid and submandibular/sublingual saliva

Histatins are small proteins of human glandular saliva that have antifungal properties. Recent studies show that oral candidal infections increase with age, suggesting an age-associated compromise in oral host defence. Here, the effect of age and of physiological gland stimulation on the concentration and secretion of salivary histatins was investigated. Parotid and submandibular/sublingual salivas were collected from six young adults under unstimulated, mechanical (chewing) and gustatory (0.025 M and 0.1 M citric acid) stimulation, and the concentration and secretion of histatins was measured by cationic polyacrylamide gel electrophoresis with subsequent densitometric scanning of the stained gels. With gland stimulation, parotid saliva showed no significant increase in histatin concentration (μg/ml); however, histatin secretion (μg/min) increased up to 26-fold ( p<0.005; ANOVA). Stimulation of submandibular/sublingual saliva resulted in significant increases in both histatin concentration ( p<0.005) and secretion ( p<0.0005). Ageing effects on salivary histatins were determined in citric acid (0.1 M)-stimulated parotid and submandibular/sublingual saliva samples collected from 80 individuals (divided into four age groups having approximately equal numbers of males and females: 35–44 years; 45–54 years; 55–64 years and 65–76 years). None of the patients was taking medications or wore dentures. ANOVA showed no sex differences in histatins. Regression analysis showed significant age-associated decreases for parotid saliva histatin concentration ( p<0.002) and secretion ( p<0.002) as well as for submandibular/sublingual saliva histatin concentration ( p<0.0001) and secretion ( p<0.0001). Both saliva types showed significant ( p<0.0001) decreases in the histatin concentration per mg of total protein, suggesting a preferential decrease in salivary histatins compared to total salivary protein. These results suggest that the salivary histatin component of the oral host defence system is compromised with increasing age.

Regions in the brainstem and frontal cortex where electrical stimulation elicits parotid and submandibular saliva secretion in sheep

Acute experiments were conducted in sheep anaesthetized with sodium pentobarbital to identify regions in the brain where electrical stimulation would elicit secretion by the parotid and submandibular salivary glands. This was a prerequisite for single unit studies in the future. In the brainstem, parotid and submandibular secretions were evoked on average between 7 and 16 mm rostral to obex and from 1 to 11 mm lateral to midline, with the parotid gland being active on the caudal and the submandibular on the rostral sides of this region. Overlap of the two sites was common. The combined region was either between cranial nerves VII and IX or adjacent to either one of them. Stimulating the caudal edge of the parotid sites evoked relatively high parotid secretion rates compared with other areas whereas secretions were uniform throughout the submandibular sites. The combined sites were from 2 to 5 mm deep, the dorsal edge being 1 mm below the floor of the fourth ventricle near midline and 6 mm below it at the lateral extremes. From a dorsal perspective, their orientation was essentially in the lateral plane except that the submandibular site angled slightly rostrally from midline. Profuse parotid secretion was also consistently evoked by stimulating the frontal cortex 15–20 mm from midline and 0–15 mm under the apex. Weak submandibular responses were observed in about half of the sheep. There were no effects on either gland of stimulating the olfactory bulbs. This is the first report of the regions in the brain which increase parotid and submandibular saliva secretion in ruminants. The three-dimensional representation of both sites in the brainstem of individual animals is more precise than the composite representations published to date for other species.

Decreased parotid saliva gustin/carbonic anhydrase VI secretion: an enzyme disorder manifested by gustatory and olfactory dysfunction.

Taste and smell dysfunction has been reported to occur in patients with a variety of clinical problems. We wanted to investigate a specific group of patients in whom taste and smell dysfunction occurred putatively related to a specific biochemical abnormality in a salivary growth factor [gustin/carbonic anhydrase (CA) VI] considered responsible for maintenance of taste bud function. Eighteen patients developed loss and/or distortion of taste and smell after an acute influenza-type illness. They were evaluated clinically, by psychophysical tests of taste and smell function, by measurement of parotid salivary gustin/CAVI by a radioimmunoassay and by measurement of serum, urine, and salivary zinc. Biopsies of circumvallate papillae were obtained in 6 patients and examined by transmission electron microscopy. Similar studies were performed in 55 asymptomatic volunteers with biopsies of circumvallate papillae performed in 4. Taste and smell acuity were impaired in patients compared with healthy volunteers and parotid gustin/CAVI, salivary, and serum zinc concentrations were lower in patients than in healthy volunteers. Taste buds in circumvallate papillae of patients exhibited severe vacuolization, cellular degeneration, and absence of dense extracellular material. These results describe a clinical disorder formulated as a syndrome of hyposmia (decreased smell acuity), hypogeusia (decreased taste acuity), dysosmia (distorted smell function), dysgeusia (distorted taste function), and decreased secretion of parotid saliva gustin/CAVI with associated pathological changes in taste bud anatomy. Because gustin/CAVI is found in humans only in parotid saliva and has been associated with taste bud growth and development these results suggest that inhibition of synthesis of gustin/CAVI is associated with development of taste bud abnormalities and thereby loss of taste function.

Decreased Parotid Saliva Gustin/Carbonic Anhydrase VI Secretion: An Enzyme Disorder Manifested by Gustatory and Olfactory Dysfunction

Background: Taste and smell dysfunction has been reported to occur in patients with a variety of clinical problems. We wanted to investigate a specific group of patients in whom taste and smell dysfunction occurred putatively related to a specific biochemical abnormality in a salivary growth factor [gustinlcarbonic anhydrase (CA) VI] considered responsible for maintenance of taste bud function. Methods: Eighteen patients developed loss and/or distortion of taste and smell after an acute influenza-type illness. They were evaluated clinically, by psychophysical tests of taste and smell function, by measurement of parotid salivary gustin/CAVI by a radioimmunoassay and by measurement of serum, urine, and salivary zinc. Biopsies of circumvallate papillae were obtained in 6 patients and examined by transmission electron microscopy. Similar studies were performed in 55 asymptomatic volunteers with biopsies of circumvallate papillae performed in 4. Results: Taste and smell acuity were impaired in patients compared with healthy volunteers and parotid gustin/CAVI, salivary, and serum zinc concentrations were lower in patients than in healthy volunteers. Taste buds in circumvallate papillae of patients exhibited severe vacuolization, cellular degeneration, and absence of dense extracellular material. Conclusions: These results describe a clinical disorder formulated as a syndrome of hyposmia (decreased smell acuity), hypogeusia (decreased taste acuity), dysosmia (distorted smell function), dysgeusia (distorted taste function), and decreased secretion of parotid saliva gustin/CAVI with associated pathological changes in taste bud anatomy. Because gustin/CAVI is found in humans only in parotid saliva and has been associated with taste bud growth and development these results suggest that inhibition of synthesis of gustin/CAVI is associated with development of taste bud abnormalities and thereby loss of taste function.

Non-adrenergic, non-cholinergic reflex secretion of parotid saliva in rats elicited by mastication and acid applied on the tongue.

Chewing and acid on the tongue evoked a flow of saliva from the duct-cannulated parotid gland of the conscious rat despite pretreatment with atropine and adrenoceptor antagonists. This non-adrenergic, non-cholinergic (NANC) response depended on an intact parasympathetic innervation and was abolished by a tachykinin antagonist. The present findings are consistent with a physiological role for the secretory NANC mechanisms of the salivary glands.

The masticatory-parotid salivary reflex in edentulous subjects.

The parotid-masticatory salivary reflex has been studied in edentulous subjects. Salivary flow was recorded by siting a modified Lashley cup over the orifice of the parotid duct on one side of the mouth. Subjects chewed on small pieces of silicone rubber with their complete dentures for 1 min periods which resulted in a reflex secretion of parotid saliva. The secretion was greatest when the subject chewed on the same side of the mouth (ipsilateral) as the salivary flow was recorded. Less salivary flow resulted when the subjects chewed on the opposite side of the mouth (contralateral). Anaesthesia of the mucosa of the maxillary and mandibular denture-bearing area was achieved by placing a thin layer of anaesthetic ointment in the fitting surface of the dentures on the side ipsilateral to the Lashley cup. This resulted in a reduction of salivary flow in response to similar chewing cycles. The results confirmed the presence of a parotid-masticatory salivary reflex in edentulous subjects which appears similar in many respects to that of dentate subjects. It is likely that receptors in the oral mucosa are stimulated when an edentulous subject masticates with complete dentures and that activity in these mechanoreceptive neurones results in the reflex salivary secretion.

Age-related changes in salivary antibodies to commensal oral and gut biota.

The prevalence of mucosally derived infections appears to increase with age, suggesting dysfunction at the mucosal surfaces. The present investigation was undertaken to examine any age-related changes in secretion rates and concentrations of secretory antibodies in whole and parotid saliva in a healthy adult population. A total of 116 subjects were subdivided into the following age groups: 20-39 years, 40-59 years, 60-79 years and 80 years and over. Specific immunoglobulin A (IgA), IgG and IgM antibodies in whole and parotid saliva to Streptococcus mutans (serotype c), Actinomyces viscosus NCTC 10951, and Escherichia coli NCTC 10418 were quantified by enzyme-linked immunosorbent assay. IgA antibodies to all three organisms examined increased with age in both whole and parotid saliva, whereas IgG antibody levels to S. mutans in whole saliva were significantly decreased with age. IgG antibodies to E. coli in parotid saliva were reduced in older age groups. IgM antibody levels to S. mutans were reduced with age in both secretions, whereas IgM antibodies to A. viscosus were greatest in the oldest age groups. No significant changes with age were observed in salivary IgM antibody levels to E. coli. No significant reduction in the secretion rates of IgA antibodies were observed in parotid or whole saliva, whereas IgG and IgM antibody secretion rates to all three microorganisms were reduced in most age groups in both whole and parotid saliva. The results of this investigation have demonstrated age-related changes with salivary antibodies, but, whereas salivary IgG and IgM antibodies showed decreases, salivary IgA levels generally increased with age. This suggests that the ability to form IgA antibody responses is not impaired with increased age, and that secretion rates and functional properties of antibodies may be as important as concentrations in protection against mucosal infective diseases.

Influences of emotion upon parotid secretion in human

Fluid of the parotid gland was collected from seven human subjects during sleep and four subjects during wakefulness. It was continuously weighed during collection on an electronic balance. The weight value was processed on line by a personal computer, and circadian rhythm in connection with the flow rate of saliva was studied. One subject showed no secretion of saliva throughout sleep, but in the other subjects, saliva was secreted, although it was slight. There was no difference between the flow rate in rapid eye movement (REM) sleep and non-REM sleep. Every subject during wakefulness showed a flow rate in a range from a very high value to one almost equal to the value during sleep. The flow rate during wakefulness varied greatly, and there seemed to be no rhythmic pattern to it. With the aid of auditory or visual stimuli etc., the influence of emotional state upon parotid secretion was investigated in 12 subjects. It was found that the flow rate decreased significantly from an intense, passionate state to a relaxed, pleasant state, to a tense or uneasy state and was lowest in a passive, indifferent state, being almost the same as that during sleep. These findings suggest that secretion of parotid saliva depends more on emotional state than circadian rhythm.

Fluid and protein secretion from ferret submandibular and parotid glands in response to sympathetic nerve stimulation or administration of sympathomimetics.

Electrical stimulation of the sympathetic innervation evoked secretion of submandibular and parotid saliva. By changing the mode of stimulation from a continuous to an intermittent one the fluid response increased and glandular blood flow improved. The volumes from the submandibular glands were larger than those from the parotid glands and further, the protein concentration of submandibular saliva was higher than that of parotid saliva. Adrenaline, isoprenaline and phenylephrine evoked larger fluid responses from submandibular than from parotid glands. However, the fluid response was small compared to the parasympathetic one. Substance P-evoked saliva was used as carrier for protein released by sympathetic nerve stimulation or administration of adrenaline and isoprenaline. In vitro tissues of submandibular and parotid glands responded to adrenaline with a dose-dependent release of protein. Taken together, the analytical pharmacology performed in vivo and in vitro, and including the antagonists phentolamine, dihydroergotamine, propranolol and metoprolol, showed that in submandibular glands, alpha(alpha 1)adrenoceptors were predominantly involved in fluid secretion and beta(beta 1)-adrenoceptors predominantly involved in protein secretion. In parotid glands, fluid secretion seemed solely to depend on alpha(alpha 1)-adrenoceptors, while beta(beta 1)-adrenoceptors seemed almost solely involved in protein secretion.