Increase In Salivary Secretion Research Articles

D-Serine Increases Release of Acetylcholine in Rat Submandibular Glands.

d-serine has been observed in submandibular gland tissue in rats, but its functions remain to be clarified. Oral administration of d-serine, but not l-serine, increased its concentrations in the submandibular gland and pilocarpine-induced salivary secretion. In vivo microdialysis was used to collect the d- and l-enantiomers of amino acids from local interstitial fluid in the rat submandibular gland. The proportion of the d-form of serine in interstitial fluid was higher than that in plasma or saliva. Perfusion of the rat submandibular gland with d-serine and l-glutamic acid via the submandibular gland artery resulted in a significant increase in salivary secretion after stimulation of muscarinic receptors with carbachol. In vivo microdialysis applied to the submandibular glands of rats showed that infusion of d-serine along with l-glutamate through the microdialysis probe significantly elevated acetylcholine levels in local interstitial fluids in the submandibular glands of anesthetized rats as compared to that with l-glutamate alone in an N-methyl-d-aspartate receptor glycine site antagonist-sensitive manner. These results indicate that d-serine augments salivary secretion by increasing acetylcholine release in the salivary glands.

Facial Exercise as an Effort to Improve Quality of Life in Elderly People With Xerostomia at Posyandu, Gedawang Village Banyumanik, Semarang

ABSTRACT Background: The function of the organs of the elderly as they get older will decrease (organ degeneration), both due to natural factors and due to disease. An estimated 30% of seniors aged 65 years and older have decreased saliva production. Decreased saliva production causes complaints of dry mouth which is often known as xerostomia. This situation is caused by atrophy of the salivary glands (saliva) which will reduce salivary production and change its composition. The decreased salivary secretion will cause discomfort in the oral cavity, pain, and increased rates of dental caries and oral infections. Facial gymnastics is the act of giving massage to the facial area from top to bottom around the cheeks, mouth, and chin, this activity can stimulate the function of the oral cavity.Research objective: to analyze the effectiveness of facial exercises on the quality of life of elderly people with xerostomia.Research Methods: Quasi-experimental with pre-test and post-test design, a sample of 30 elderly people with xerostomia. Facial exercise treatment was carried out for 30 days, measurements were carried out using the Xerostomia Related Quality of Life Scale (XeQoLS). Questionnaires were given before and after treatment.Results: The results showed that after doing facial exercises there was an increase in salivary secretion from an average of 0.6 ml/per minute to 1.1 ml/per minute, and the results of the paired t-test p-value = 0.000. The majority of respondents had a low quality of life of 53% and after doing facial exercises the majority of respondents had a high quality of life of 57%, with the results of the paired t-test p-value = 0.000. This can happen because the implementation of facial exercises gets mechanical stimulation. The stimulation given can increase the flow of salivary secretion which directly affects the increase in saliva volume. The normal salivary secretion will cause a sense of comfort in the oral cavity, thereby increasing the quality of life of the elderly.

Development and optimization of tibezonium iodide and lignocaine hydrochloride containing novel mucoadhesive buccal tablets: a pharmacokinetic investigation among healthy humans

Objective It is clinically important to deliver a sustained-release mucoadhesive dosage of local anesthetic and antimicrobial agents for pain control. The current study aimed to develop and evaluate chitosan (CHI) based buccal mucoadhesive delivery for the local release of tibezonium iodide (TBN) and lignocaine hydrochloride (LGN). Methods Direct compression technique was employed, aided by other mucoadhesive polymers like hydroxypropylmethylcellulose (HPMC) and sodium alginate (SA) and evaluated for physicochemical and in vivo character. Results Fourier transform infrared spectral analysis (FTIR), powdered X-ray diffraction (XRPD), and differential scanning calorimetry (DSC) absence of physical interaction between ingredients. The physical parameters complied with USP specifications for all formulations. Optimum swellability (551.9%) was offered from formulation TL15, containing 30% SA. The highest ex vivo mucoadhesive strength (24.79 g) and time (18.39 h) was found with TL8. Formulation TL8 also exhibited maximum in vivo residence time (11.37 h). Almost complete drug release at 6 h was possessed by formulation TL5 (HPMC and CHI, 20% each) for TBN (99.98%) and LGN (99.06%). The optimized formulation TL5 exhibited dosage stability up to 6 months at 75% relative humidity and retained drug contents. TL5 was well tolerated by the volunteers with no inflammation, pain or irritation found. Almost 73% of volunteers reported an increase in salivary secretion. The first-order salivary C max of TBN and LGN were found as 16.02 and 7.80 µg/mL within 4 h, respectively. Conclusion Therefore, the sustained release mucoadhesive dosage form of TBN and LGN can be an effective and alternative option to conventional delivery.

Selected Molecular Mechanisms Involved in the Parasite⁻Host System Hymenolepis diminuta⁻Rattus norvegicus.

The rat tapeworm Hymenolepis diminuta is a parasite of the small intestine of rodents (mainly mice and rats), and accidentally humans. It is classified as a non-invasive tapeworm due to the lack of hooks on the tapeworm’s scolex, which could cause mechanical damage to host tissues. However, many studies have shown that metabolites secreted by H. diminuta interfere with the functioning of the host’s gastrointestinal tract, causing an increase in salivary secretion, suppression of gastric acid secretion, and an increase in the trypsin activity in the duodenum chyme. Our work presents the biochemical and molecular mechanisms of a parasite-host interaction, including the influence on ion transport and host intestinal microflora, morphology and biochemical parameters of blood, secretion of antioxidant enzymes, expression of Toll-like receptors, mechanisms of immune response, as well as the expression and activity of cyclooxygenases. We emphasize the interrelations between the parasite and the host at the cellular level resulting from the direct impact of the parasite as well as host defense reactions that lead to changes in the host’s tissues and organs.

Differences in salivary secretory function between patients with erosive esophagitis and those with nonerosive reflux disease

It has been speculated that impaired salivary flow contributes to abnormal acid clearance in patients with erosive esophagitis (EE). For easy and objective assessment of salivary function, we developed a salivary gland blood flow measurement technique using continuous-wave Doppler sonography. In the present study, we evaluated the salivary secretory function in patients with EE and those with nonerosive reflux disease (NERD) using this method. Doppler waveform analysis was performed on the facial artery to assess blood inflow to the submandibular gland of 30 healthy subjects (HS). Blood flow was compared before and after secretory stimulation with 1mL of lemon juice. Saliva was simultaneously collected and weighed before and after stimulation. Continuous-wave Doppler sonography was also performed in patients with EE and NERD. The size of the submandibular gland was compared in 26 patients with EE, 41 patients with NERD, and 86 HS. The submandibular gland blood flow increased after stimulation in all HS. Both within-day and day-to-day reproducibility were good. There was a significant correlation between the percent increase in the maximum velocity and the percent increase in salivary secretion. Although the size of the submandibular gland was not significantly different among the three groups, the percent increase in the maximum velocity in patients with EE was significantly smaller than that in HS. We have established an easy method of assessing salivary function in daily practice. This study revealed that a decrease in salivary secretory function is involved in the pathology of EE.

THU0166 Rebamipide in the treatment of xerostomia in sjægren’s syndrome: Randomized placebo-controlled study

BackgroundXerostomia is a major distressing symptom in Sjögren’s syndrome (SS). Persistent dryness of the mouth causes oral pain, discomfort and significantly interferes with the quality of life. Rebamipide, in addition...

Efficacy and safety of rebamipide for the treatment of dry mouth symptoms in patients with Sjögren’s syndrome: a double-blind placebo-controlled multicenter trial

The effects of rebamipide on dry mouth and salivary secretion in Sjögren’s syndrome patients were investigated in a double-blind placebo-controlled study. Rebamipide (100 mg TID) or placebo was administered for eight weeks and patient-assessed improvement of dry mouth and increase in salivary secretion measured by the Saxon test were evaluated. At two, four, and eight weeks, dry mouth improvement rates were, respectively, 26.0, 44.0, and 46.9% for rebamipide and 20.0, 27.1, and 39.1% for placebo, and mean increases in salivary secretion were, respectively, 0.14, 0.24, and 0.35 g for rebamipide and 0.03, 0.09, and 0.17 g for placebo, indicating higher values in the rebamipide group for both parameters at all timepoints but no significant differences between the two groups. Analysis by baseline characteristics suggested a statistically significant salivary secretion increasing effect of rebamipide in cases of primary Sjögren’s syndrome. No difference in the incidence of adverse events was seen between the two groups, confirming the safety of rebamipide. As a salivary secretion increasing effect was strongly suggested in cases of primary Sjögren’s syndrome, further study on the administration of rebamipide for the treatment of dry mouth in patients with Sjögren’s syndrome is required.

Pilocarpine-induced salivary fluid secretion in the perfused submandibular gland of the rat

Xerostomia is the symptom of dry mouth often seen in patients who receive head and neck radiation therapy or in patients who have Sjögren's syndrome. The primary treatment to relieve xerostomia symptom is oral administration of pilocarpine, a parasympathomimetic agent with muscarinic action. Increase in salivary secretion induced by systemic administration of pilocarpine is considered to be mediated by actions on muscarinic cholinergic receptors in the central nervous system and salivary glands. In this study, we investigated the direct effect of pilocarpine on salivary fluid secretion in the isolated, perfused rat submandibular gland. Pilocarpine provoked salivary fluid secretion in a dose-dependent manner. The Na(+)-channel blocker tetrodotoxin had almost no effect on the pilocarpine-induced salivary fluid secretion, indicating that pilocarpine directly stimulates submandibular gland. Pilocarpine induced an increase in intracellular Ca(2+) concentration in dispersed submandibular gland cells at 37 degrees C, but not 25 degrees C. The salivary fluid secretion induced by pilocarpine was consisted of a rapid and transient phase and a subsequent sustained phase, which profile was different from that evoked by carbachol, another typical muscarinic agonist. Pilocarpine also induced Lucifer yellow secretion via paracellular route.

Efficacy and safety of rebamipide for the treatment of dry mouth symptoms in patients with Sjögren’s syndrome: a double-blind placebo-controlled multicenter trial

The effects of rebamipide on dry mouth and salivary secretion in Sjögren's syndrome patients were investigated in a double-blind placebo-controlled study. Rebamipide (100 mg TID) or placebo was administered for eight weeks and patient-assessed improvement of dry mouth and increase in salivary secretion measured by the Saxon test were evaluated. At two, four, and eight weeks, dry mouth improvement rates were, respectively, 26.0, 44.0, and 46.9% for rebamipide and 20.0, 27.1, and 39.1% for placebo, and mean increases in salivary secretion were, respectively, 0.14, 0.24, and 0.35 g for rebamipide and 0.03, 0.09, and 0.17 g for placebo, indicating higher values in the rebamipide group for both parameters at all timepoints but no significant differences between the two groups. Analysis by baseline characteristics suggested a statistically significant salivary secretion increasing effect of rebamipide in cases of primary Sjögren's syndrome. No difference in the incidence of adverse events was seen between the two groups, confirming the safety of rebamipide. As a salivary secretion increasing effect was strongly suggested in cases of primary Sjögren's syndrome, further study on the administration of rebamipide for the treatment of dry mouth in patients with Sjögren's syndrome is required.

Expression of BMP7 is associated with resistance to diabetic stress: Comparison among mouse salivary glands

We determined mRNA levels of bone morphogenetic protein 7 (BMP7), a growth and differentiation factor belonging to the transforming growth factor-β superfamily, in the salivary glands of mice with streptozotocin (200 mg/kg, i.p.)-induced diabetes. We also examined the effects of BMP7 on secretion of saliva and degenerative change in salivary glands in diabetic mice. In normal mice, BMP7 mRNA levels were high in the submandibular gland and low in the parotid gland, while in diabetic mice, levels were significantly decreased in the parotid gland, but not in the submandibular gland. No significant difference was observed in mRNA levels of BMP receptors between normal and diabetic mice. In diabetic mice, pilocarpine (4 mg/kg, i.p.)-stimulated salivary secretion showed a remarkable decrease in both parotid and submandibular gland, although degree of reduction was smaller in the latter. Notable degeneration with vacuolation and atrophy was also found in parotid gland, whereas degeneration of submandibular gland was slight. Administration of BMP7 (50 and 100 µg/kg, i.v.) in diabetic mice induced a significant increase in salivary secretion, with rate of recovery higher in parotid gland than in submandibular gland. In diabetic mice, BMP7 also exhibited a powerful protective effect in degenerated salivary gland, especially in parotid gland. These results suggest that BMP7 acts to prevent diabetic damage in salivary gland, and that its cytoprotective effect is closely correlated with mRNA levels in tissue.

Chitosan-containing gum chewing accelerates antibacterial effect with an increase in salivary secretion

Objectives This study was designed to confirm the mechanical efficacy of chewing chitosan-containing gum to suppress the growth of oral bacteria compared to a mouth rinse, and to demonstrate the increased salivary secretion due to chewing chitosan-containing gum. Method Twelve healthy subjects were recruited from among the staff and students of Nagasaki University School of Dentistry. For the slab of gum study, the subjects chewed chitosan-containing gum for 5 min and then rested for 5 min. For the testing of the chitosan mouth rinse solution, the subjects gargled 10 mL of solution for 30 s followed by resting for 9 min 30 s. These protocols were continuously repeated five times for 50 min on the same day. For the salivary secretion experiment, the gum chewing was repeated three times per day for 2 days. Results The amount of oral bacteria in the subjects who chewed chitosan-containing gum significantly decreased during all three sampling times except at 60 min for total bacteria in comparison to those in the rinse group. Chitosan-containing gum chewing also significantly increased the secretion of saliva. Conclusions Chitosan-containing gum chewing has a greater antibacterial effect and it also increases salivary secretion. The present findings strongly indicate that the application of natural materials such as chitosan is useful for both oral health and the quality of life.

Comparative in vivo uroselectivity profiles of anticholinergics, tested in a novel anesthetized rabbit model

The aim of this study was to describe a new experimental animal model for simultaneous measurement of carbachol-induced increase in intravesical pressure and salivary secretion in rabbits. Further, we also compared the in vivo potency and urinary bladder versus salivary gland selectivity profiles of Oxybutynin, Tolterodine, Solifenacin and Darifenacin. The intravesical pressure and salivary secretion were evoked by intra-arterial injection of carbachol (1.5 microg/kg). The carbachol-induced increase in intravesical pressure and salivation was simultaneously recorded before and after increasing doses of test drugs administered intravenously. The basal mean changes in intravesical pressure and salivation subsequent to carbachol administration were in the range of 6.7-7.5 mm Hg and 0.5-0.7 g respectively. Repeated administration of vehicle did not elicit any appreciable changes in intravesical pressure and salivary secretion to carbachol administration from the basal values till 3 h. All the test drugs exhibited a dose-dependent inhibition of carbachol-induced increase in intravesical pressure and salivary secretion. Darifenacin demonstrated a greater potency compared to other muscarinic receptor antagonists for inhibiting carbachol-induced increase in intravesical pressure. It also exhibited functional selectivity for the urinary bladder versus salivary gland. In contrast, Oxybutynin was functionally more selective in inhibiting carbachol-induced increase in salivary secretion. The observed urinary bladder versus salivary selectivity values were 0.6+/-0.2, 1.1+/-0.2, 1.7+/-0.5, and 2.3+/-0.5 for Oxybutynin, Tolterodine, Solifenacin and Darifenacin respectively. These results suggest that the functional selectivity of muscarinic receptor antagonists between urinary bladder and salivary glands can be readily detected in this model. Thus rabbits may represent a useful animal model for evaluating putative bladder selective muscarinic receptor antagonists for the treatment of overactive bladder.

Functional relationship between subfornical organ cholinergic stimulation and nitrergic activation influencing cardiovascular and body fluid homeostasis

We have studied the effects of l-NG-nitro arginine methyl esther ( l-NAME), l-arginine (LAR), inhibitor and a donating nitric oxide agent on the alterations of salivary flow, water intake, arterial blood pressure (MAP) and heart rate (HR) induced by the injection pilocarpine into the subfornical organ (SFO). Rats (Holtzman 250–300 g) were anesthetized with 2, 2, 2-tribromoethanol (20 mg/100 kg b. wt.) and a stainless steel cannula were implanted into their SFO. The volume of injection was 0.2 μl. The amount of saliva secretion was studied over a 5-min period. Pilocarpine (40 μg), l-NAME (40 μg) and LAR (30 μg) were used in all experiments for the injection into the SFO. Pilocarpine (10, 20, 40, 80 and 160 μg) injected into SFO elicited a concentration-dependent increase in salivary secretion. l-NAME injected prior to pilocarpine into the SFO increased salivary secretion and water intake due to the effect of pilocarpine. LAR injected prior to pilocarpine into the SFO attenuated the salivary secretion and water intake. Pilocarpine, injected into the SFO increased the MAP and decreased heart rate (HR). l-NAME injected prior to pilocarpine into the SFO potentiated the pressor effect of pilocarpine with a decrease in HR. LAR injected into the SFO prior to pilocarpine attenuated the increase in MAP with no changes in HR. The present study suggests that the SFO nitrergic cells interfere in the cholinergic pathways implicated in the control of salivary secretion, fluid and cardiovascular homeostasis.

The relationship between salivary secretion rate and masticatory efficiency.

In order to elucidate the relationship between the salivary secretion rate and masticatory efficiency, experimental hypo- and hyper-salivation were produced by the administration of atropine sulphate presenting an anticholinergic effect and pilocarpine hydrochloride having a muscarine effect orally in 10 healthy fully dentates. To confirm the pharmaceutical effect of these drugs, the unstimulated whole salivary secretion rate during 10 min, and masticatory efficiency using the sieve method were measured before and after medication. The unstimulated whole salivary secretion rate during 10 min decreased significantly by the administration of atropine sulphate (P < 0.05), and increased significantly by pilocarpine hydrochloride (P < 0.01). The masticatory efficiency after atropine sulphate medication was significantly lower than that before (P < 0.01). The increase in salivary secretion by pilocarpine hydrochloride did not lead to a higher masticatory efficiency. The evidence supports the understanding that saliva plays an important role in masticatory function.

Nitric oxide of the supraoptic nucleus influences the salivary secretion, sodium renal excretion, urinary volume and arterial blood pressure induced by pilocarpine

Male Holtzman rats weighting 200–250 g were anesthetized with zoletil 50 mg/Kg (tiletamine chloridrate 125.0 mg and zolazepan chloridrate 125.0 mg) into quadriceps muscle and stainless steel cannulas were implanted into their supraoptic nucleus (SON). We investigated the effects of the injection into the supraoptic nucleus (SON) of FK 409, a nitric oxide donor, and N W-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor (NOS), on the salivary secretion, arterial blood pressure, sodium excretion and urinary volume induced by pilocarpine, which was injected into SON. The drugs were injected in 0.5 μl volume over 30–60 s. Controls was injected with a similar volume of 0.15 M NaCl. FK 409 and L-NAME were injected at doses of 20 μg/0.5 μl and 40 μg/0.5 μl respectively. The amount of saliva secretion was studied over a five-minute period after injection of pilocarpine into SON. Injection of pilocarpine (10, 20, 40, 80, 160 μg/μl) into SON produced a dose-dependent increase in salivary secretion. L-NAME was injected into SON prior to the injection of pilocarpine into SON, producing an increase in salivary secretion due to the effect of pilocarpine. FK 409 injected into SON attenuating the increase in salivary secretion induced by pilocarpine. Mean arterial pressure (MAP) increase after injections of pilocarpine into the SON. L-NAME injected into the SON prior to injection of pilocarpine into SON increased the MAP. FK 409 injected into the SON prior to pilocarpine attenuated the effect of pilocarpine on MAP. Pilocarpine (0.5 μmol/0.5 μl) injected into the SON induced an increase in sodium and urinary excretion. L-NAME injected prior to pilocarpine into the SON increased the urinary sodium excretion and urinary volume induced by pilocarpine. FK 409 injected prior to pilocarpine into the SON decreased the sodium excretion and urinary volume induced by pilocarpine. All these roles of pilocarpine depend on the release of nitric oxide into the SON. In summary the present results show: a) SON is involved in pilocarpine-induced salivation; b) that mechanism involves increase in MAP, sodium excretion and urinary volume.

Role of nitric oxide of the median preoptic nucleus (MnPO) in the alterations of salivary flow, arterial pressure and heart rate induced by injection of pilocarpine into the MnPO and intraperitoneally.

We investigated the effect of L-NAME, a nitric oxide (NO) inhibitor and sodium nitroprusside (SNP), an NO-donating agent, on pilocarpine-induced alterations in salivary flow, mean arterial blood pressure (MAP) and heart rate (HR) in rats. Male Holtzman rats (250-300 g) were implanted with a stainless steel cannula directly into the median preoptic nucleus (MnPO). Pilocarpine (10, 20, 40, 80, 160 g) injected into the MnPO induced an increase in salivary secretion (P<0.01). Pilocarpine (1, 2, 4, 8, 16 mg/kg) ip also increased salivary secretion (P<0.01). Injection of L-NAME (40 g) into the MnPO prior to pilocarpine (10, 20, 40, 80, 160 g) injected into the MnPO or ip (1, 2, 4, 8, 16 mg/kg) increased salivary secretion (P<0.01). SNP (30 g) injected into the MnPO or ip prior to pilocarpine attenuated salivary secretion (P<0.01). Pilocarpine (40 g) injection into the MnPO increased MAP and decreased HR (P<0.01). Pilocarpine (4 mg/kg body weight) ip produced a decrease in MAP and an increase in HR (P<0.01). Injection of L-NAME (40 g) into the MnPO prior to pilocarpine potentiated the increase in MAP and reduced HR (P<0.01). SNP (30 g) injected into the MnPO prior to pilocarpine attenuated (100%) the effect of pilocarpine on MAP, with no effect on HR. Administration of L-NAME (40 g) into the MnPO potentiated the effect of pilocarpine injected ip. SNP (30 g) injected into the MnPO attenuated the effect of ip pilocarpine on MAP and HR. The present study suggests that in the rat MnPO 1) NO is important for the effects of pilocarpine on salivary flow, and 2) pilocarpine interferes with blood pressure and HR (side effects of pilocarpine), that is attenuated by NO.

Novel evidence that nitric oxide of the medial septal area influences the salivary secretion induced by pilocarpine

Our studies have focused on the effect of injection of L-NAME and sodium nitroprussiate (SNP) on the salivary secretion, arterial blood pressure, sodium excretion and urinary volume induced by pilocarpine which was injected into the medial septal area (MSA). Rats were anesthetized with urethane (1.25 g/kg b. wt.) and a stainless steel cannula was implanted into their MSA. The amount of saliva secretion was studied over a five-minute period after injection of pilocarpine into MSA. Injection of pilocarpine (10, 20, 40, 80, 160 μg/μl) into MSA produced a dose-dependent increase in salivary secretion. L-NG-nitro arginine methyl-esther (L-NAME) (40 μg/μl), a nitric oxide (NO) synthase inhibitor, was injected into MSA prior to the injection of pilocarpine into MSA, producing an increase in salivary secretion due to the effect of pilocarpine. Sodium nitroprussiate (SNP) (30 μg/μl) was injected into MSA prior to the injection of pilocarpine into MSA attenuating the increase in salivary secretion induced by pilocarpine. Medial arterial pressure (MAP) increase after injections of pilocarpine into the MSA. L-NAME injected into the MSA prior to injection of pilocarpine into MSA increased the MAP. SNP injected into the MSA prior to pilocarpine attenuated the effect of pilocarpine on MAP. Pilocarpine (40 ug/ul) injected into the MAS induced an increase in sodium and urinary excretion. L-NAME injected prior to pilocarpine into the MSA increased the urinary sodium excretion and urinary volume induced by pilocarpine. SNP injected prior to pilocarpine into the MSA decreased the sodium excretion and urinary volume induced by pilocarpine. All these roles of pilocarpine depend on the release of nitric oxide into the MSA. We may also conclude that the MSA is involved with the cholinergic excitatory mechanism that induce salivary secretion, increase in MAP and increase in sodium excretion and urinary volume.

Role of nitric oxide and β-adrenoceptors of the central nervous system on the salivary flow induced by pilocarpine injection into the lateral ventricle

Our studies have focused on the effect of l- NG-nitroarginine methyl ester ( l-NAME), an inhibitor of nitric oxide synthase (NOS), and l-arginine, the substrate of NOS, on salivary secretion induced by the administration of pilocarpine into the lateral cerebral ventricle (LV) of rats. The present study has also investigated the role of the β-adrenergic agonists and antagonist injected into LV on the salivary secretion elicited by the injection of pilocarpine into LV. Male Holtzman rats with a stainless-steel cannula implanted into the LV were used. The amount of salivary secretion was studied over a 7-min period after injection of pilocarpine, isoproterenol, propranolol, salbutamol, salmeterol, l-NAME and l-arginine. The injection of pilocarpine (10, 20, 40, 80 and 160 μg/μl) into LV produced a dose-dependent increase in salivary secretion. The injection of l-NAME (40 μg/μl) into LV alone produced an increase in salivary secretion. The injection of l-NAME into LV previous to the injection of pilocarpine produced an increase in salivary secretion. l-Arginine (30 μg/μl) injected alone into LV produced no change in salivary secretion. l-Arginine injected into LV attenuated pilocarpine-induced salivary secretion. The isoproterenol (40 nmol/μl) injected into LV increased the salivary secretion. When injected previous to pilocarpine at a dose of 20 and 40 μg/μl, isoproterenol produced an additive effect on pilocarpine-induced salivary secretion. The 40-nmol/μl dose of propranolol injected alone or previous to pilocarpine into LV attenuated the pilocarpine-induced salivary secretion. The injection of salbutamol (40 nmol/μl), a specific β-2 agonist, injected alone into LV produced no change in salivary secretion and when injected previous to pilocarpine produced an increase in salivary secretion. The 40-nmol/μl dose of salmeterol, a long-acting β-2 agonist, injected into LV alone or previous to pilocarpine produced no change in salivary secretion. The results have shown that central injections of l-NAME and l-arginine interfere with the salivary secretion, which implies that might participate in pilocarpine-induced salivary secretion. The interaction between cholinergic and β-adrenergic receptors of the central nervous system (CNS) for the control of salivary secretion can also be postulated.

Cyclosporin A: Effects on the Secretory Process and Noradrenergic Activity in the Submandibular Gland of the Rat

Objectives: The aim of the present work was to study the effect of long-term cyclosporine (CSA) administration on norepinephrine (NE) metabolism and adrenergic-evoked secretion in the rat submandibular gland (SMG). Methods: Dose-response curves to adrenergic agonists (methoxamine, isoproterenol, NE) were performed in control and CSA (10 and 30 mg/kg every 2 days for 1 month)-treated rats after SMG duct cannulation. In SMG tissue neuronal NE uptake, release, synthesis and endogenous content were determined. In addition phosphoinositide intracellular signaling was also investigated. Results: CSA administration caused an increase in salivary secretion evoked by methoxamine (α-adrenergic agonist) and NE but failed to modify salivation evoked by β-adrenergic stimulation (isoproterenol). Long-term CSA administration decreased NE release and synthesis whereas it enhanced the amine uptake and phosphoinositide hydrolysis in the SMG. Conclusions: The administration of CSA for 30 days induced salivary gland sensitization likely mediated by diminished adrenergic input. Present results suggest that the decreased sympathetic activity evoked by long-term CSA administration in the rat SMG may lead to sensitization of the gland supported by increased phosphoinositide hydrolysis and enhanced adrenergic-evoked salivation.

Non- N-methyl- d-aspartate receptors may mediate the transmission of emetic signals between visceral vagal afferents and the solitary nucleus in dogs

The effects of the N-methyl- d-aspartate (NMDA) and non-NMDA receptor antagonists MK-801 and NBQX, respectively, on salivary secretion and retching induced by vagal stimulation were studied in decerebrate dogs. Vagal stimulation induced an increase in salivary secretion and fictive retching. Intra-4th ventricular application of vehicle or MK-801 did not change either response, while NBQX completely abolished both responses. These results suggest that non-NMDA receptors mediate both responses in the solitary nucleus.