Submandibular secretion in the dog after intraluminal injections of amiloride

The effects of amiloride on flow rate, osmolarity, Na⁺, K⁺ and Cl^? concentrations were studied in the submandibular glands of dogs. The drug was injected in a retrograde fashion into the duct system of the gland, which was subsequently stimulated to secrete with pilocarpine. In concentrations of 10^?4 and 10^?3 M, amiloride increased the Na⁺ concentration but did not significantly alter the K⁺ concentration of saliva. A slight decrease in Cl^? concentration was observed at high flow rates after 10^?4 M amiloride, but otherwise the drug did not significantly affect the Cl^? concentration of stimulated salivary secretion. The diuretic has a measurable mucosal (luminal) effect on Na⁺ transport in dog submandibular gland, which is similar to that reported in amphibian epithelia. Its lack of effect on K⁺ excretion differs from findings reported in other epithelial structures, where it has a marked K⁺-sparing effect. The drug increased the salivary osmolarity in a fashion similar to Na⁺, a finding that suggests a dissociation between Na⁺ and water transport in salivary duct epithelium.     

Sialochemistry and cortisol levels in patients with Sjogren's syndrome

Oral Diseases (2012) 18 , 255–259 Objectives: (i) To determine whether salivary cortisol and electrolyte levels differ between patients with Sjogren’s syndrome (SjS) and healthy individuals. (ii) To assess correlations between whole‐saliva cortisol and some clinical manifestations in patients with SjS. Methods: A total of 24 healthy women (mean age 49.3 ± 9.8) served as controls (C) vis‐à‐vis 17 patients with SjS (mean age 55.5 ± 15.7). Salivary cortisol concentration was determined, and sialochemistry analysis was performed. Results: Significantly lower saliva flow rates and higher salivary chloride (Cl^?), potassium (K⁺), and Ca²⁺ levels were found in the SjS group. No significant differences or correlations were found in other parameters, including sodium (Na⁺), magnesium (Mg²⁺), phosphate (^?), urea (U), and salivary cortisol levels. Conclusion: Increased whole‐salivary output of Cl^? and K⁺ in SjS may reflect release from apoptotic rests of acinar cells after secondary necrosis. Normal levels of salivary Na⁺, Mg²⁺, and ^? argue against concentration effect, deranged tubular function or cortisol (mineralocorticosteroid) effect as the cause for these findings. Increased salivary Ca²⁺ levels probably reflect leakage of plasma Ca²⁺ through the injured oral mucosa in SjS. In spite of disease‐associated stress, salivary cortisol, a stress biomarker, was not increased, suggesting insufficient hypothalamus–pituitary–adrenal (HPA) axis response and/or local consumption of cortisol by lymphocyte infiltrates.     

Salivary anticandidal activity and saliva composition in an HIV‐infected cohort

This study investigated salivary anticandidal activity and salivary composition in stimulated whole saliva of 18 advanced HIV‐infected patients and compared these values to healthy controls. Stimulated whole saliva from HIV‐infected patients showed decreased anticandidal activity. The flow rate was reduced by 40% as compared with controls. The saliva flow rate for HIV‐infected patients who had recoverable yeast in their saliva was reduced as compared to HIV‐infected patients without recoverable yeast. For HIV‐infected patients, the saliva concentrations of lactoferrin, secretory IgA and Cl^? were increased while the secretion rate of lysozyme, total protein and K⁺ were reduced. There was no difference in any parameter as a function of taking the antifungal drug fluconazole. There was no association between salivary anticandidal activity and any salivary component. This study shows reduced anticandidal activity and salivary flow rate in HIV‐infected patients. These alterations may contribute to their increased incidence of oral candidal infections.     

Fluid and electrolyte secretion from the isolated,perfused submandibular and sublingual glands of the rat

Isolated preparations of the rat submandibular gland secreted when perfused at a rate of 3 ml/min with physiological salt solutions containing glucose and either acetylcholine (10^?9 to 10^?4 M) or pilocarpine (10^?7 to 10^?3 M). The maximum secretory response was 250 μl g^?1 min^?1 with acetylcholine (10^?6 M) and 130 μl g^?1 min^?1 with pilocarpine (10^?6 M). Higher agonist concentrations usually resulted in smaller secretory responses. The response to continued stimulation showed a slow decline, although it was more sustained than with a similar preparation of the rabbit submandibular gland. The excretion curves for Na, K, Ca, Cl and HCO₃ evoked by the two parasympatho-mimetic agonists were similar to those reported from in-vivo experiments. Ouabain (10^?3 M), the substitution of Na by Li or the omission of K in the perfusion solution markedly inhibited the secretory response from the isolated, perfused-gland preparation. Partial substitution of the perfusate Na with choline caused only partial inhibition of secretion, but decreased Na and increased Ca and K concentrations in saliva. It is concluded that the perfused-gland preparation functions normally with respect to the secretion of fluid and electrolytes, and offers a suitable vehicle for investigation of the salivary secretory process. The sublingual gland secreted in response to pilocarpine. The maximum secretory rate was 130 μl g^?1 min^?1 and the saliva was poor in Na and Cl and rich in K, HCO₃ and Ca.     

The Electrolyte and Water Secretion Mechanism

The currently accepted salivary gland secretion model describes the process of fluid secretion as the coordinated action of water and ion channels and transporters. The secretion of electrolytes and water by salivary glands is thought to be activated by an agonist-induced increase in the intracellular free [Ca²⁺] and to be driven by transepithelial chloride movement. The Cl^- transport is supported by upregulation of several ion transporters, K⁺ and Cl^- channels, and the Na⁺/K⁺-ATPase. This review will focus on the details of the transport mechanisms as well as recent developments in confirming the molecular identities of the involved transporter and channel proteins.     

Characteristics of neurokinin A-induced salivary fluid secretion in perfused rat submandibular gland

Tachykinins such as neurokinin A (NKA) and substance P have been demonstrated to induce salivary fluid secretion in vivo. However, characteristics of salivary fluid secretion induced by tachykinins in salivary glands have not been well elucidated. In this study, the effects of the tachykinin NKA on salivary fluid secretion were investigated in isolated, perfused rat submandibular gland. NKA provoked salivary fluid secretion, which consisted of transient and sustained phases, in a dose-dependent manner. In fura-2-loaded dispersed cells of the rat submandibular gland, the doses of NKA in which induced salivary fluid secretion caused an increase in intracellular Ca²⁺ concentration. When Ca²⁺ was removed from the perfusate to examine the effect of Ca²⁺ mobilization on NKA-induced fluid secretion, only the transient salivary fluid secretion occurred. When the gland was perfused with the Ca²⁺-free perfusate containing the intracellular Ca²⁺ chelator BAPTA-AM, NKA failed to induce salivary fluid secretion. NKA also induced an increase in oxygen consumption, but which was reduced by the removal of Ca²⁺ from perfusate. Salivary fluid is secreted via transcellular and paracellular pathways in acinar cells of salivary glands. To examine the contribution of paracellular pathway to NKA-induced salivary fluid secretion, the glands were perfused with a perfusate containing Lucifer yellow (LY), a cellular impermeable substance, and then were stimulated with NKA, which provoked secretion of LY in the saliva. These results suggest that the NKA-induced salivary fluid secretion is Ca²⁺-dependent and that the paracellular pathway contributes to the secretion.     

Cholinergic autoantibodies from primary Sjögren’s syndrome modulate submandibular gland Na+/K+‐ATPase activity via prostaglandin E2 and cyclic AMP

Passafaro D, Reina S, Sterin‐Borda L, Borda E. Cholinergic autoantibodies from primary Sjögren’s syndrome modulate submandibular gland Na ⁺ /K ⁺ ‐ATPase activity via prostaglandin E ₂ and cyclic AMP. Eur J Oral Sci 2010; 118: 131–138. © 2010 The Authors. Journal compilation © 2010 Eur J Oral Sci We demonstrate that patients with primary Sjögren’s syndrome (pSS) produce functional IgG autoantibodies that interact with the glandular M₃ muscarinic acetylcholine receptors (mAChRs). These autoantibodies act as a partial muscarinic agonist, increasing prostaglandin E₂ (PGE₂) and cyclic AMP production through modifying Na⁺/K⁺‐ATPase activity, but also interfere with the secretory effect of the parasympathetic neurotransmitter. The IgG from patients with pSS has two effects on the submandibular gland. On the one hand, it may act as an inducer of the proinflammatory molecule (PGE₂) that, in turn, inhibits Na⁺/K⁺‐ATPase activity. On the other hand, it plays a role in the pathogenesis of dry mouth, abolishing the Na⁺/K⁺‐ATPase inhibition and the net K⁺ efflux stimulation of the salivary gland in response to the authentic agonist pilocarpine, decreasing salivary fluid production.     

Primary Sjögren''s syndrome: salivary gland function and clinical oral findings

OBJECTIVE: To evaluate salivary gland function, saliva composition and oral findings in patients with primary Sjogren's syndrome (pSS) subdivided into patients with and without focus score ≤1 (FS) and/or antibodies to SSA/SSB (AB) as well as in healthy controls. SUBJECTS AND METHODS: Unstimulated (UWS) and chewing stimulated (SWS) whole saliva, and stimulated parotid saliva (SPS) were collected in 16 patients fulfilling the European classification criteria for pSS subdivided into those with FS and/or AB (n= 8) and those without FS and AB (n= 8), and in age-matched (n= 14) and young healthy controls (n= 13).UWS and SWS were analysed for Na⁺ and K⁺.SPS was analysed for Na⁺, K⁺, statherin, and proline-rich proteins (PRPs).Sicca symptoms, DMFT/DMFS, plaque (PI) and gingival (GI) scores, periodontal pocket depth (PPD), and mucosal status were recorded. RESULTS: The young healthy controls had lower UWS as compared to the aged controls (P= 0.03).However, the aged controls had higher DMFT/DMFS (P < 0.001) and PI, GI and PPD (P < 0.01).Patients with FS and/or AB generally had lower saliva secretory rates than patients without FS and/or AB (P= 0.01 for UWS and SPS) and age-matched healthy controls (P= 0.001). There was no significant difference in the content of Na⁺ and K⁺, statherin and PRPs between groupS. Patients with FS and/or AB had the highest frequency of oral mucosal changes and higher DMFT/DMFS than patients without FS and/or AB and healthy controls (P < 0.01).However, PI, GI, and PPD did not differ significantly. CONCLUSION: Patients with FS and/or AB had lower salivary secretory rates, higher DMFT/DMFS, and more oral mucosal changes than patients without FS and/or AB.Additionally, data suggest that salivary gland function in healthy individuals do not decrease with age.     

Effects of monensin on fluid and electrolyte secretion by the isolated, perfused rat submandibular gland

The sodium ionophore monensin caused a secretory response which was characterized by small volumes of saliva with high K and HCO3 and low Na and Cl concentrations. When added to the perfusate concomitantly with acetylcholine, it reduced the volume of saliva secreted in 60 min by 74 per cent and caused an increase in salivary Na and Cl concentrations at low rates of flow. When glands were exposed to monensin for 30 min prior to acetylcholine stimulus, the fluid secretory response to the secretagogue was inhibited 96 per cent and the electrolyte composition of that secretion had higher Na and Cl and lower K and HCO3 concentrations than the monensin-induced one. The small secretory response induced by monensin is likely to be the result of Na entry into the salivary cells, which is of such magnitude that it rapidly dissipates the transmembrane Na gradient. This may affect the Na, K pump responsible for the maintenance of this gradient and the ion-transport systems dependent on it.     

Specific expression of salivary maxi-K channel variant is augmented in diabetic mice

Background and objective

A genetically diabetic mouse strain (db/db) exhibits severe obesity and a syndrome resembling human non-insulin-dependent diabetes mellitus. Our histological study of submandibular glands revealed that the size and area of the granular convoluted tubules was substantially decreased in db/db mice. We hypothesized that this structural difference reflected a specific alteration in salivary duct function.

Methods

The saliva evoked by pilocarpine was used for the measurement of ion concentrations, and submandibular glands were dissected out for the immunohistochemistry and real-time PCR study.

Results

The K⁺ concentration of the salivary secretion was higher in db/db than in control m+/m+ mice, while neither saliva volume nor the concentrations of Na⁺ or Cl⁻ differed between these strains. In db/db mice (vs. m+/m+ mice): quantitative PCR analysis revealed an increased mRNA expression of large-conductance Ca²⁺-activated K⁺ (maxi-K) channels, immunohistochemistry revealed an increase in the luminal surface expression of the maxi-K channel protein, and a particularly interesting finding was that there was a substantial increase in the salivary tissue-specific splice variant ParSlo.

Conclusion

These results suggest that in db/db mice, the K⁺ content of saliva may be elevated due to an expression of a maxi-K channel variant, which results from a modification of ductal structure. General significance: Our data may shed some light on the mechanism responsible for determining the dynamics of salivary K⁺ concentration increased in diabetic patients.     

Effects of cyclic nucleotide derivatives on acetylcholine-induced secretion from isolated, perfused rat submandibular salivary glands

The effects of dibutyryl cAMP, 8-bromo-cGMP, 3-isobutyl-1-methyl xanthine (MIX) and isoproterenol were examined. When administered simultaneously with acetylcholine (10(-6) M) in concentrations of 10(-5) M, both isoproterenol and cAMP reduced fluid secretion (16 and 31 per cent, respectively) and enhanced the decay in rate of flow with time, while cGMP and MIX increased salivary volumes (25 and 19 per cent, respectively). Isoproterenol-decreased Na and Cl and increased K and residual anion concentrations. These effects, except for increased K, were also observed with MIX, cAMP and cGMP did not significantly affect cation concentrations but reduced Cl and increased residual anion, although to a lesser extent than isoproterenol or MIX. The cyclic nucleotides did not affect the flow of saliva when added to the perfusate for 40 min after 40 min of acetylcholine stimulation. Prior exposure to cGMP increased the volume of saliva secreted after re-exposure to acetylcholine alone and both cGMP and cAMP increased the Na and reduced the K concentration of the stimulated secretion. These results suggest that cyclic nucleotides are involved in salivary fluid and electrolyte secretion and can modulate the effects of cholinergic stimuli. cGMP may be involved mainly in fluid secretion and, as salivary fluid originates almost exclusively in salivary acini, it may exert its action in acinar cells and activate specific components of the mechanism of primary secretion. cAMP may be primarily involved in transductal electrolyte transport, and may also inhibit certain parts of the fluid secretory mechanism, or reduce the effectiveness of cholinergic stimuli in activating them.(ABSTRACT TRUNCATED AT 250 WORDS)     

The biphasic effect of extracellular glucose concentration on carbachol‐induced fluid secretion from mouse submandibular glands

Cholinergic agonists evoke elevations of the cytoplasmic free‐calcium concentration ([Ca²⁺]_i) to stimulate fluid secretion in salivary glands. Salivary flow rates are significantly reduced in diabetic patients. However, it remains elusive how salivary secretion is impaired in diabetes. Here, we used an ex vivo submandibular gland perfusion technique to characterize the dependency of salivary flow rates on extracellular glucose concentration and activities of glucose transporters expressed in the glands. The cholinergic agonist carbachol (CCh) induced sustained fluid secretion, the rates of which were modulated by the extracellular glucose concentration in a biphasic manner. Both lowering the extracellular glucose concentration to less than 2.5 mM and elevating it to higher than 5 mM resulted in decreased CCh‐induced fluid secretion. The CCh‐induced salivary flow was suppressed by phlorizin, an inhibitor of the sodium–glucose cotransporter 1 (SGLT1) located basolaterally in submandibular acinar cells, which is altered at the protein expression level in diabetic animal models. Our data suggest that SGLT1‐mediated glucose uptake in acinar cells is required to maintain the fluid secretion by sustaining Cl^? secretion in real‐time. High extracellular glucose levels may suppress the CCh‐induced secretion of salivary fluid by altering the activities of ion channels and transporters downstream of [Ca²⁺]_i signals.     

EMF measurements across hydroxyapatite membranes

An attempt was made to develop models applicable to the study of ionic transport in dental enamel. Membranes of hydroxyapatite, made by compression of the powdered salt, were mounted on the septum of concentration cells. Electrical potential differences, PD, were measured across the membranes using solutions of CaCl₂, NaCl, KCl, and potassium and sodium phosphates. With CaCl₂, the membrane acquired a net positive charge and the PD values were close to those expected for an ideal permselective membrane. High permselectivity and a net negative charge on the membrane were observed with solutions of Na₂HPO₄ and K₂HPO₄. The PD values obtained with NaCl and KCl solutions were close to those calculated for the junction potentials of the electrolytes; thus, for these uni-univalent salts the membrane behaved as an inert porous barrier. The permselective behaviour was interpreted in terms of sorption of Ca²⁺ and phosphate ions probably related to defects in the hydroxyapatite crystals. The lack of interaction with K⁺, Na⁺, and Cl^? was ascribed to the reduced ionic charge and the relatively large pore sizes of the membrane.When the membranes were mounted on an intraoral device and exposed to the oral environment prior to the PD measurements, the electrochemical behaviour of the membrane changed drastically. The PD values obtained were consistent with the acquisition of a net negative charge on the membrane surface. This negative charge decreased during the initial time (several hours) of measurements but persisted if saliva was added to the electrolyte solutions. A rapid adsorption of salivary proteins is thought to be responsible for the change of the membrane properties after intraoral exposure.It was concluded that any model developed to study ionic transport in dental enamel should include the interactions with the salivary constituents and the presence of the tooth pellicle.     

Calcium-stimulated ATPase of dog submandibular gland

A Ca^2?-stimulated ATPase present in a microsomal fraction prepared from canine submandibular glands was investigated. The Ca²⁺ concentration for half maximal activation of the enzyme was about 0.3 mM. Addition of Mg²⁺ to incubation media containing Ca²⁺ decreased the ATPase activity. The presence of neither Na⁺ nor K⁺ is required for Ca²⁺-activation of the enzyme. Also, Ca²⁺ will not substitute for Mg²⁺ in the Mg²⁺-dependent (Na⁺ + K⁺)-ATPase reaction. The Ca²⁺-activation was not appreciably affected by ouabain (10^?4M), but was inhibited by about 50 per cent by 5 × 10^?3M ethacrynic acid. These studies provide a possible enzymatic basis for the calcium uptake by salivary gland microsomes that has been reported by other workers.     

Purines,a new class of agonists in salivary glands?

The response of rat submandibular glands to extracellular purines was tested. In crude cellular suspensions, ATP increased the [Ca²⁺]_i mostly by promoting uptake of extracellular calcium. ATP caused the pH_i to drop, a response blocked by chloride channel inhibitors. ATP also inhibited the basal and isoproterenol-stimulated activity of the Na⁺-K⁺-2Cl-cotransporter. These effects were reproduced by benzoyl-ATP, an agonist of ionotropic purinoceptors. In pure ductal suspensions, ATP activated a metabotropic P2Y₁ purinergic receptor coupled to phospholipase C and opened a non-specific cation channel coupled to a P2X₇ receptor. Activation of these receptors stimulated a Ca²⁺-dependent and a Ca²⁺-independent phospholipase A₂, the latter resulting in kallikrein secretion.We conclude that purinergic agonists can modulate the activity of both acinar and ductal phases of secretion. Activation of metabotropic receptors coupled to phospholipase C could lead to responses resembling those to muscarinic or adrenergic agonists. Activation of ionotropic receptors could stimulate new intracellular responses also involved in secretory function.     

Roles of CLCA and CFTR in electrolyte re-absorption from rat saliva

A molecular basis for Cl- re-absorption has not been well-characterized in salivary ductal cells. Previously, we found strong expression of a rat homologue proposed to be Ca2+-dependent Cl- channels (rCLCA) in the intralobular ducts of the rat submandibular gland. To address the question as to whether rCLCA and cystic fibrosis transmembrane conductance regulator (CFTR) are involved in Cl- re-absorption, we evaluated the electrolyte content of saliva from glands pre-treated with a small interfering RNA (siRNA). Retrograde injection into a given submandibular duct of an siRNA designed to knock down either rCLCA or CFTR reduced the expression of each of the proteins. rCLCA and CFTR siRNAs significantly increased Cl- concentration in the final saliva during pilocarpine stimulation. These results represent the first in vivo evidence for a physiological significance of rCLCA, along with CFTR, in transepithelial Cl- transport in the ductal system of the rat submandibular gland.     

Characterization of a microsomal fraction from rabbit parotid gland: Partial separation of alkaline phosphatase from Na,K-ATPase

Subfractionation of the 140,000 g_max pellet from the rabbit parotid gland revealed 3 fractions. Both linear and discontinuous sucrose-density gradients were used to separate a region of high-density particles with considerable mitochondria, a middle region rich in Na⁺,K⁺-ATPase (sodium-potassium activated adenosine triphosphatase) and a low-density (top) region with elevated alkaline phosphatase. The top and middle fractions appeared to represent subfractions of plasma-membrane enriched membranes. Treatment of these 2 gradient fractions with low concentrations of sodium dodecyl sulphate confirmed that the middle fraction was preferentially enriched in Na⁺,K⁺-ATPase. Thus, alkaline phosphatase-enriched membranes are at least partially separable from Na⁺,K⁺-ATPase-enriched membranes. Separation of alkaline phosphatase from Na⁺,K⁺-ATPase may be an important purification step in future work involving isolation of plasma membranes of secretory cells, as both alkaline phosphatase and Na⁺,K⁺-ATPase have been used as plasma-membrane markers in the parotid gland. The present findings demonstrate that considerable caution should be exercised in defining the purity of plasma-membrane fractions from the parotid gland in view of the heterogeneity of the plasma-membrane enriched fraction.     

In-vitro release of K+ from the developing submandibular gland of early postnatal rats

The release studied by incubating tissue slices in an enriched, oxygenated medium in the presence and absence of secretagogues indicated that slices from 1-day-old rats released K⁺ in response to carbamylcholine, but not in response to epinephrine. The response to carbamylcholine was dose-related, with a 12.6 ± 1.3 per cent release at a concentration of 2 × 10^?5M. Epinephrine did not induce K⁺ release in concentrations from 2 × 10^?7 to 2 × 10^?5M. Glands from 7- and 14-day-old rats released a similar amount as those of new-borns in response to carbamylcholine and by 21 days of age the glands released 21.5 ± 1.9 per cent of their K⁺ content upon exposure to 2 × 10^?5M carbamylcholine. A response to epinephrine (2 × 10^?5M) was first detected at 14 days of age, when the slices released 8.3 ± 1.2 per cent of their K⁺. Slices of 21-day-old rats showed a 17.9 ± 1.3 per cent K⁺ release in response to this dose. As in adult glands, the net amount of K⁺ released by the developing postnatal gland seems to be the result of two opposing mechanisms, a passive efflux and an active re-uptake which depends on the activation of an ouabain-sensitive Na⁺-K⁺ -ATPase. The passive efflux component was similar in glands from different postnatal ages and was enhanced by secretagogues. The extent of active uptake, on the other hand, decreased with increasing postnatal age. As in the adult, the net release of K⁺ depended on the presence of Ca2⁺ in the incubation medium, but the sensitivity of the response to Ca²⁺ omission varied in accord with the age of the animals and with the stimulant used. It is speculated that proacinar and terminal tubular cells may be involved in K⁺ release in the early postnatal period.     

Effects of 4,4′-diisothiocyano-2,2′-stilbene disulphonic acid and amiloride on salivary secretion by isolated, perfused rat submandibular glands

Isolated submandibular glands of adult rats were perfused through the arterial system with oxygenated, HCO3-containing or HCO3-free physiological salt solutions. Secretion of saliva was then induced with acetylcholine (10(-6) M) in the absence or presence of the ion-transport inhibitors 4,4'-diisothiocyano-2,2'-stilbene disulphonic acid (DIDS), furosemide or amiloride. In HCO3-containing perfusates, 10(-4) M DIDS enhanced the initial secretory response (maximum rate of flow increased 18 per cent), but reduced the overall volume of saliva secreted in a 60-min period by 47 per cent. Furosemide (10(-3) M) alone reduced the volume of saliva by 73 per cent and, in combination with 10(-4) M DIDS, by 82 per cent. Amiloride (10(-3) M) caused a 68 per cent reduction in salivary volumes. Replacement of perfusate HCO3 with HEPES did not affect acetylcholine-induced secretion but enhanced the effects of the transport inhibitors, so that total volume of secretion was reduced 94 per cent by furosemide, 55 per cent by DIDS and 80 per cent by amiloride. In HCO3-containing perfusates, DIDS caused a 30-50 per cent increase in salivary Na+ and residual anion (Na + K - Cl) concentrations but amiloride induced a marked increase in salivary Na+ and Cl- concentrations and a decrease in salivary K+ concentrations. Furosemide caused a marked decrease in salivary Cl- concentrations and a marked increase in residual anions. These effects were similar but of smaller magnitude in HCO3-free, HEPES-containing perfusates.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nerve interactions in salivary glands

In the salivary reflex, not only secretory cells are activated, but also myo-epithelial cells are contracted to support these cells and promote the flow of saliva, and blood vessels dilate to meet the increased demands of the tissues. The various effector cells often receive nerves from both parts of the autonomic system, and interactions may occur when the nerves act on the same type of effector, or on different types of effectors. While in an experiment electrical stimulation of the sympathetic trunk may decrease a parasympathetic salivary flow by causing marked vasoconstriction, this does not occur in the salivary reflex, since the vasoconstrictors do not take part. On the contrary, the normal sympathetic vasoconstrictor tone of the resting gland is easily overcome by activity in parasympathetic vasodilator nerves when secretion starts. Pronounced synergism can be demonstrated between sympathetic and parasympathetic secretory nerves. In dogs, for instance, in which sympathetic secretion is beta-adrenoceptor-mediated, this is marked in the case of fluid secretion. In rats and rabbits, in which beta-receptors elicit secretion of amylase, the potentiating interaction among the nerves is striking when amylase secretion is considered. Even the random release of acetylcholine from the post-ganglionic parasympathetic axons, by itself insufficient to evoke secretion, can increase the sympathetic effects. Motor nerves interact with secretory nerves by causing myo-epithelial contraction, mechanically promoting secretion. Interactions between the nerves in their long-term regulatory function on the sensitivity of the acinar secretory and myo-epithelial cells can also be demonstrated.