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PubMed2006

Oral hydration, parotid salivation and the perceived pleasantness of small water volumes.

Previous studies have suggested that the preference for drinking cold water is increased when the drinker has a dry mouth. In a first experiment, we investigated whether a positive shift in preference would occur for small water volumes (0.75 ml and 1.5 ml) at 8, 16 or 25 degrees C, delivered into a mouth that had been dried using a warmed airflow, versus a normally hydrated mouth. Subjects rated the perceived wetness (or dryness) of their mouth, and the perceived pleasantness (or unpleasantness) of the water samples, using a labeled magnitude scale. Cooler water samples were preferred, and consistent with previous research, this preference was slightly enhanced when the subject's mouth was dried. The coldest water sample led to significantly wetter mouthfeel than the other two less cold samples, consistent with the possibility that the coldest water increased the rate of salivation. However, a second experiment found that although the rate of parotid salivation was increased if the mouth had been dried using a warm airflow, the different water temperatures did not induce different rates of parotid salivation. This indicates that enhanced preference for cold water when the mouth is dry is not invariably based in the reward gained from mouth rewetting via increased parotid saliva flow.

Adult↗

PubMed1975

Food-reinforced inhibition of conditioned salivation in dogs.

Twelve dogs salivated to a tone that was followed by food, but not to a noise for which there was an added response dependency. The noise was followed by food if and only if they did not salivate. The addition of this response dependency vitiated the classically conditioned response to the noise. A yoked-control group of 6 dogs receiving the same sequences of stimuli and food salivated to both the tone and noise stimuli.

Acoustic Stimulation↗

PubMed1999

Effects of captopril and bradykinin on chorda tympani-induced salivation in cat.

The effects of captopril and bradykinin on chorda tympani-induced salivation were studied in the submandibular gland of anesthetized cat. Captopril and bradykinin, but not des-Arg9-bradykinin, increased salivation evoked by electrical stimulation of chorda tympani. These potentiated effects of captopril and bradykinin were suppressed by Hoe-140, a kinin B2 receptor antagonist, or by concomitant addition of N(G)-nitro arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, and aspirin, a cyclooxygenase inhibitor. It appears that captopril potentiates chorda tympani-induced salivation through endogenously accumulated bradykinin, which acts on kinin B2 receptors, mediating production of nitric oxide and cyclooxygenase products.

Adrenergic beta-Antagonists↗

PubMed1983

Quantification of salivation, nasal secretion and tearing in man.

The purpose of this study has been to establish a battery of tests of autonomic functions: Quantification of submandibular/sublingual salivation, nasal secretion and tearing on both sides. The tests were performed in a control group of 20 healthy students. We used a parasympathomimetic drug, pilocarpine 0.1 mg/kg body weight, to stimulate the different secretory functions. Saliva was collected with a pair of dentistry spiral suctions. Tearing was assessed with Schirmer's test tapes. Nasal secretion was quantified using Schirmer's test tapes, too. Nasal secretion and salivation on average was fairly symmetrical, whereas there was some asymmetry in tearing (which may be artificial). In single individuals, there may be considerable asymmetry in salivation as well. This test battery will be used in the study of possible autonomic dysfunctions in patients with unilateral headache.

Adolescent↗

PubMed1984

Autonomic disorders in cluster headache, with special reference to salivation, nasal secretion and tearing.

Attacks of cluster headache are often associated with symptoms of an autonomic nature. A test battery allowing quantitation of salivation, nasal secretion and tearing has been employed. Fourteen patients examined under basal conditions hardly differed from a group of controls (N = 20). After stimulation with pilocarpine the patients responded like the controls. During attacks we found minimal bilateral salivation, but an increase of tearing and nasal secretion, mostly on the symptomatic side. These results correspond with those found in CPH. The finding of the minimal salivation is consistent with the notion that the headache attacks are associated with increased sympathico-tonus. The results may suggest that the complexity of the innervation pattern of the different secretory organs examined is more marked than hitherto known.

Adult↗

PubMed1980

The long-term effect of energy intake on salivation, hunger, and appetite ratings, and estimates of energy intake in obese patients.

The relationship between salivation, hunger, appetite, and estimates of energy intake was examined in female obese inpatients undergoing a course of weight reduction. On a constant low-energy intake (800 kcal/day) salivation, hunger, and appetite scores all declined. Estimates of energy intake did not. Sixteen different subjects were fed 1000 kcal/day for seven days, 500 kcal/day for seven days, and 1000 kcal/day for seven days. After acclimatization to the diet for a minimum of five days, salivation was directly related to energy intake; hunger and appetite ratings did not change significantly; and estimates of energy intake were sensitive to the decrease but not increase in energy intake. The limitations of each method of assessment are discussed.

Adolescent↗

PubMed1988

Anticholinergic side-effects of antidepressants: studies of the inhibition of salivation.

Studies of the peripheral anticholinergic effects of antidepressants initiated by Ole J. Rafaelsen are reviewed. They were all cross-over trials, either in patients who received continuous medication or in which continuous medication was temporarily discontinued, or in volunteers given single doses. Anticholinergic effects were evaluated from the inhibition of salivation rate measured by a tampon method. In essence, the studies revealed that 1) the method was sufficiently reliable and sensitive, 2) inhibition of salivation by tricyclic antidepressants persisted during long-term treatment, and 3) the newer antidepressants Nomifensine, Zimeldine, Mianserin, Citalopram, and Femoxetine were less potent as to anticholinergic effects than tricyclic antidepressants. The results of the studies reviewed have generally been in good agreement with similar studies of other centers and with clinical between-group studies. Other authors have found a sufficient specificity of salivation rate measurements for anticholinergic effects, but other methods, for instance based on heart rate measurements, may prove to be more specific.

Antidepressive Agents↗

PubMedDate not supplied

Central and peripheral mediation of hypothermia, tremor and salivation induced by muscarinic agonists in mice.

UNLABELLED: Hypothermia, tremor and salivation induced by muscarinic cholinergic agonists were studied in mice. Oxotremorine-M (quarternary agonist) shows high potency after intracerebroventricular administration, but the potency is low after subcutaneous administration. Oxotremorine potency (non-quarternary agonist) is higher after intracerebroventricular administration than after subcutaneous administration. Scopolamine and atropine (non-quarternary antagonists) antagonize oxotremorine-induced effects more potently after intracerebroventricular than subcutaneous administration. The quarternary antagonists N-methylscopolamine (NMS) and N-methylatropine (NMA) potently antagonize oxotremorine-induced salivation after both subcutaneous and intracerebroventricular administration. Hypothermia is antagonized partially (20-40%) over a large dose range after subcutaneous administration. In ex vivo receptor-binding studies of rat brain tissue, oxotremorine, scopolamine and atropine administered subcutaneously dose-dependently displace 3H-oxotremorine-M. Oxotremorine-M and NMS displace 3H-oxotremorine-M by 21% and 35%, respectively; NMA is ineffective. IN CONCLUSION: Muscarinic cholinergic-mediated tremor is centrally regulated; hypothermia involves both a central and a peripheral component, the peripheral regulation being relatively less important than the central; central and peripheral regulation of salivation are equally important. Penetration of the blood brain barrier by oxotremorine-M and NMS is shown in the ex vivo binding studies.

Animals↗

PubMed1980

Regulation of body volume by salivation in a tick challenged with fluid loads.

Injection into the hemolymph of 1.2% NaCl, 11.2% sucrose, 2.3% urea (all approximately isosmotic to hemolymph), or distilled water induced salivary fluid secretion in the ixodid tick Amblyomma hebraeum Koch. Saline gave the largest response at high doses. Injection of hyperosmotic NaCL into the hemolymph did not induce salivation but led to the drinking of distilled water in amounts sufficient to dilute the salt load to isosmolarity. Atropine only partially inhibited salivation induced by NaCl, sucrose, and distilled water. Reserpine markedly inhibited salivation induced by NaCl. We propose that at least two sensory pathways (one cholinergic, one not) converge on the secretory nerve. The physiological significance of the cholinergic pathway is not known. The other pathway probably mediates the regulation of hemolymph volume, possibly via stretch receptors, but its transmitter is not known.

Animals↗

PubMed1995

Effects of clonidine and yohimbine on parasympathetic reflex salivation and vasodilatation in cat SMG.

The present experiments were designed to examine the site of action of the alpha 2-adrenoceptor agonist, clonidine, and the alpha 2-antagonist, yohimbine, on the salivary secretion response to parasympathetic and sympathetic stimulation in the cat submandibular gland (SMG). The parasympathetic reflex salivary secretion was significantly affected by both clonidine and yohimbine (clonidine reduced and yohimbine increased the amount of saliva secreted) while the reflex vasodilator response was not affected by either agent. No degree of methacholine-induced salivation was affected by prior treatment with either clonidine or yohimbine. The salivation elicited by facial nerve root stimulation was markedly reduced by clonidine but potentiated by yohimbine. Prior treatment with scopolamine completely abolished the salivary secretion induced by either methacholine or facial nerve root stimulation. Clonidine and yohimbine had no effect on SMG salivation elicited by sympathetic stimulation. These results indicate that the alpha 2-agonist and antagonist act specifically on parasympathetic salivary fibers but have no effect on parasympathetic vasodilator fibers. They thus suggest that postganglionic parasympathetic innervation is differentiated into salivary and vasodilator fibers.

Animals↗

PubMed1999

[Effects of propiverine hydrochloride (propiverine) on the muscarinic receptor binding affinity in guinea pig tissues and on salivation in conscious dogs].

Propiverine is a drug for the treatment of incontinence and pollakiuria. Such micturitional disorders are principally caused by a hyperactive bladder. The effects of propiverine, its active metabolite, 1-methyl-4-piperidyl benzilate N-oxide (DPr-P-4 (N-->O)), oxybutynin and terodiline on muscarinic receptors in guinea pig urinary bladder, salivary glands, cerebral cortex, ileal longitudinal muscle and heart were compared. Both propiverine and DPr-P-4 (N-->O) competitively inhibited specific binding of 3H-quinuclidinyl benzilate (3H-QNB) to membrane fractions of these tissues. Oxybutynin, terodiline, pirenzepine and atropine also competitively inhibited the binding of 3H-QNB. The order of these drugs in terms of their affinity for muscarinic receptors was as follows: atropine > oxybutynin > pirenzepine, DPr-P-4 (N-->O), terodiline > propiverine. Propiverine and DPr-P-4 (N-->O) had no selectivity for muscarinic receptors in these tissues, the same as atropine. In contrast, pirenzepine, a M1-selective drug, had 10.1 times greater affinity for muscarinic receptors in the cerebral cortex than in urinary bladder, and the affinity of oxybutynin for muscarinic receptors in salivary glands and in cerebral cortex was 10.9 times and 13.9 times higher, respectively, than in urinary bladder. The affinity of terodiline for muscarinic receptors in the cerebral cortex was 4.4 times higher than in urinary bladder. In this study, the effect of propiverine and oxybutynin on pilocarpine (1 mg/kg, s.c.)-induced salivation in conscious dogs was also compared. Propiverine (5 mg/kg, i.v.) had no effect on pilocarpine-induced salivation, whereas oxybutynin (0.1 mg-0.5 mg/kg, i.v.) inhibited it significantly and dose-dependently. The ID50 values (95% confidence limits) for propiverine and oxybutynin during the 20 min after intravenous administration were 6.88 mg/kg (4.71-15.67) and 0.154 mg/kg (0.115-0.205), respectively. These findings suggest that although propiverine, its active metabolite DPr-P-4 (N-->O), oxybutynin and terodiline competitively inhibit the binding of 3H-QNB to muscarinic receptors, the affinity of these drugs for the muscarinic receptors of these tissues is very different and that propiverine has less effect on salivation than oxybutynin.

Animals↗

PubMed1977

Influence of food on the effect of propantheline and L-hyoscyamine on salivation.

The absorption of a quartenary (propantheline, 30 mg) and a tetiary (1-hyoscyamine, 0.8 mg) anticholinergic compound was studied in 8 healthy volunteers by measuring the effects on salivation. Both compounds were administered as rapidly disintegrating tablets, 1-hyoscyamine also in a slow-release formulation (Egazil Durules). The three preparations and placebo were administered under fasting conditions and with a standardized light meal using a randomized cross-over design. Salivation measurement were performed with a citric acid stimulation method every hour for 10 hours. In the fasting patient, all three anticholinergic test preparations decreased the salivation significantly. When taken with food, the effect of propantheline was almost abolished, while the effects of the 1-hyoscyamine preparations were uninfluenced. It was concluded that the clinical effects of proprantheline might be extremely varying depending how the drug is taken in relation to meals. In contrast the clinical effects of 1-hyoscyamine seem to be independent of food intake.

Adolescent↗

PubMedDate not supplied

[Conidioned reflex and polarization salivation].

The paper outlines some characteristics of salivation arising under the action of DC anode on the parietal areas of the dog's head. It is suggested that peculiarities and characteristics of salivation induced by a DC anode coincide with those described with regard to conditioned salivation.

Animals↗

PubMed1979

[Vegetative parameters under the effect of ouabain (g-strophanthin) in endogenous depressive patients. 1. The salivation rate].

In 7 healthy test persons and in 17 endogenous depressive patients the salivations rate was measured in a survey investigation with the SHP-test. The salivation rate of healthy test persons is constant. In endogenous depressive patients it develops a diminishing of depression depth under treatment with Ouabain (g-Strophanthin) between the 6th and the 12th day which is connected with reduction of the drive diminishing and the restauration of mood. The effective salivation rate is gaining. Possible principles of the influence of Ouabain are discussed.

Depression↗

PubMed1982

Salivation patterns of obese and normal subjects.

The salivation patterns of a group of nine obese and a group of 14 non-obese subjects were studied. Palatable food was presented and salivary responses were measured under two different conditions. In one condition, the subjects expected to eat, and in the other condition did not expect to eat. It was hypothesized that the obese group would exhibit a salivation pattern different from the non-obese group, and that this salivation pattern would be unrelated to whether or not eating was permitted. This hypothesis was not confirmed; no differences were found between the two groups. These findings conflict with those of earlier investigators and possible reasons for this are discussed.

Cues↗

PubMed1995

A modified method for quantitative measurements of cholinergic and adrenergic sialogogue-induced salivation in mice.

A modified procedure based on that reported by Richter is described for the quantitative measurement of salivation induced by sialogogues in mice. As a new immobilizing technique for mice, the present method uses a combination of light anesthesia produced by a low dose (1.0 g/kg, i.p.) of urethane and a fixing plate, instead of deep anesthesia induced by a high dose (1.8 g/kg, i.p.) of urethane. Unlike Richter's method, the immobilizing technique described here did not potentiate the toxicity of sialogogues and hence no mice died within 48 h after the end of the experiment. This method could easily measure salivation induced by cholinergic agonists (pilocarpine and bethanechol) and adrenergic agonists (phenylephrine and isoproterenol), dose-dependently. Thus, the present method may be useful for studying salivation responses induced by various types of sialogogues under less toxic experimental conditions in mice.

Animals↗

PubMed1979

Substance P stimulation of amylase release by isolated parotid cells and inhibition of substance P induction of salivation by vasoactive peptides.

Substance P stimulation of salivation in rats has been studied as has its in vitro enhancement of amylase release by isolated parotid cells. The extent of the stimulation on amylase release by isolated parotid cells was dependent upon the concentration of substance P, with the minimum effective concentration being 1 nM. The substance P effect was detectable within 1 min after incubation and lasted for at least 50 min. Substance P stimulation was demonstrable at 25--37 degrees C but not at 0 degrees C. Adrenocorticotropic hormone (ACTH), thyrotropin-releasing hormone (TRH), vasopressin and neurotensin had no effect on amylase release. These results suggest that substance P may act directly on the parotid cells. Examination of the salivary-stimulating activity of fragments of substance P showed that the C-terminal octapeptide and (pyroglutamyl)hexapeptide were active, although less potent than substance P, whereas its free acid, C-terminal tetra- and tri-peptides were inactive. Vasopressin, angiotensin II and neurotensin could inhibit substance P induced salivation, whereas TRH, ACTH and somatostatin had no effect. Amylase activity per unit volume of saliva was not changed by the injection of vasopressin, angiotensin II or neurotensin. These vasoactive peptides did not affect substance P stimulation of amylase release by isolated parotid cells. The results indicate that vasopressin, angiotensin II and neurotensin inhibit the action of substance P on salivation at sites other than the parotid cells.

Acetylcholine↗

PubMed1989

Neuropeptide K potently stimulates salivary gland secretion and potentiates substance P-induced salivation.

Neuropeptide K (NPK) is an N-terminally extended derivative of neurokinin A (NKA) that can be a final product in the posttranslational processing of beta-preprotachykinin. A rat salivation bioassay was used to demonstrate potent effects of NPK at low doses, while effects due to NKA were much weaker at higher doses. The rank order of potency of beta-preprotachykinin-derived peptides on salivation responses was NPK greater than substance P greater than NKA much greater than beta-preprotachykinin-(72-96)-peptide. The time course of the NPK response was longer than that observed with substance P. The responses elicited by NPK were blocked by the tachykinin antagonist [D-Pro2,D-Trp7,9]substance P but not by atropine. In peptide coinfusion studies, NPK strikingly potentiated the salivation responses elicited by substance P. NPK in vitro displayed a 100 times lower potency than substance P in displacing 3H-labeled substance P binding in submandibular gland membranes, a tissue rich in SP-P type (NK-1) receptors. The possible cellular mechanisms by which NPK stimulates salivary gland secretion are discussed. We conclude that NPK and substance P may be cotransmitters derived by posttranslational processing of beta-preprotachykinin.

Animals↗