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PubMed1976

Salivary Secretion in wild Glossina pallidipes Austen. (Diptera, Glossinidae).

The salivation behaviour of wild G. pallidipes obtained from Lambwe Valley and Kbwezi was studied. Salivation was measured by counting the number of salivary drops secreted per minute and measuring the sizes of the stained saliva after drawing them with a camera lucida. The results confirmed observations obtained from laboratory bred flies. The quantity of saliva secreted by tsetse flies was significantly increased as the flies became hungrier. The proportion of flies salivating also increased with intensity of hunger. Female G. pallidipes secreted significantly more saliva than the males. There was no significant difference between the quantities of saliva secreted by infected and free tsetse flies; thus there is no evidence to support the suggestion that the presence of trypanosomes in the tsetse fly stimulated it to salivate copiously. Flies having trypanosome infection in their salivary glands discharge large numbers of mature parasites in their saliva. Flies with trypanosomes in their proboscis discharged relatively few mature and immature parasites in their saliva.

Animals↗
PubMed1986

Effect of nicotine chewing gum on salivary secretion.

The effect of nicotine, placebo for nicotine or menthol-tasting chewing gums on salivation was studied in 25 healthy volunteers. The chewing of a commercial nicotine containing (2 mg) chewing gum (Nicorette) did not give a larger rate of salivation than did the chewing of a placebo chewing gum. For both types of chewing gums the rate of salivation was highest during the initial 5 min and it decreased thereafter. Menthol-tasting chewing gum gave a significantly higher amount of stimulated saliva. It is concluded that the addition of nicotine to a chewing gum does not provide an additional stimulus for salivation.

Adult↗
PubMed1987

Nonmuscarinic neurotoxicity of oxotremorine.

The ability of various treatments to prevent peripheral parasympathetic actions, central effects and lethality of the muscarinic agonist oxotremorine was studied in rats. The percentage of animals exhibiting effects of oxotremorine was dose and time dependent. The ED50 for producing lacrimation, salivation, tremor, convulsions and death was 2.5, 1.3, 1.6, 3.2 and 8.3 mg/kg i.p., respectively. Pretreatment with 5 mg/kg of atropine completely prevented all observable effects of oxotremorine at doses of 5 mg/kg and below. Doses of oxotremorine in excess of 5 mg/kg produced tremor, generalized clonic convulsions and death that could not be prevented by atropine when given at up to 160 mg/kg; lacrimation and salivation were not present in atropine-treated rats. In the presence of 40 mg/kg of atropine, ED50 values for oxotremorine were shifted more than 12-fold for lacrimation, salivation and tremor, whereas convulsions and death were maximally altered by a factor of 2. Scopolamine, benactyzine and benztropine were also incapable of completely preventing tremor, convulsions and death induced by 10 or 15 mg/kg of oxotremorine. Atropine methyl nitrate had effects comparable to atropine sulfate on lacrimation, salivation and lethality induced by oxotremorine (10 or 15 mg/kg) but had no effect on tremor or convulsions. A similar profile of atropine-insensitive effects was produced by pilocarpine and arecoline. Doses of diazepam 4 times higher (4 mg/kg) than necessary to prevent tonic-clonic convulsions induced by pentylenetetrazol were ineffective against tremor, convulsions or death produced by oxotremorine (10 or 15 mg/kg) unless given in conjunction with atropine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Alcohol cue reactivity and ad lib drinking in young men at risk for alcoholism.

Individuals at high risk for alcoholism have been hypothesized to acquire alcoholic characteristics more rapidly than those at low risk. Two studies examined reactivity to alcohol cues, a phenomenon linked to craving for alcohol in clinical alcoholics, and ad lib drinking behavior in young men at varying risk for alcoholism. In Study 1, subjects exhibited increased autonomic and subjective responses during exposure to an alcohol beverage relative to a control beverage, suggesting that alcohol cue reactivity is not merely a clinical alcoholic phenomenon but also present in more moderate drinkers. This alcohol cue reactivity, however, was unrelated to risk status. Also, high-risk subjects exhibited greater nonspecific electromyographic and skin temperature reactivity, and higher baseline salivation volume than low-risk subjects. Of special note, ad lib alcohol consumption in Study 1 was correlated with subjects' self-report of craving during exposure to the alcoholic beverage. Study 2 attempted to replicate the baseline salivation finding but results were equivocal concerning the robustness of this effect. Also in Study 2, subjects exhibited decreased salivation volume following a placebo beverage and increased salivation volume following alcohol consumption. Studies 1 and 2 compared ad lib drinking behavior in high-risk and low-risk samples, but no group differences were found.

Adult↗
PubMedDate not supplied

Differences in salivary habituation to palatable foods in bulimia nervosa patients and controls.

OBJECTIVE: Bulimia nervosa (BN) patients have been shown to experience anomalous responses to food and food cues. We investigated the response to food over time by presenting repeated food cues and measuring changes in physiological (ie, salivation) and subjective responses. METHOD: Subjects were 18 BN women and 18 matched control women. Two palatable food stimuli, regular or frozen yogurt, that varied in macronutrient composition but had similar sensory characteristics, were presented to subjects repeatedly during a laboratory session. After two baseline salivation measures, subjects were presented with eight trials of one of the two yogurts. On Trial 9 a lemon juice dishabituator was presented, with the yogurt stimulus presented again at Trial 10. RESULTS: We found that control subjects had decreased salivation after repeated food presentations. In comparison, BN subjects failed to show a decrease in salivation. The desire to binge increased over trials for the BN subjects, but remained stable for normals. CONCLUSIONS: These data suggest that salivary habituation may be abnormal in BN patients.

Adolescent↗
PubMed2006

Hypersalivation in temporal lobe epilepsy.

PURPOSE: We sought to determine whether hypersalivation helps lateralize seizure onset during complex partial seizures of temporal lobe origin. Several clinical signs, which help lateralize seizure onset, have been reported in temporal lobe epilepsy (TLE). Increased salivation only occasionally has been reported as a manifestation of partial epilepsy. METHODS: Of 590 consecutive patients admitted for video-EEG monitoring, either as a part of a presurgical evaluation of medically intractable epilepsy or for diagnosis and clarification of their paroxysmal symptoms, we identified 10 patients with ictal hypersalivation as a prominent manifestation of complex partial seizures. We reviewed the clinical features, scalp-sphenoidal video-EEG monitoring, intracarotid amytal (Wada) testing, hippocampal volumetric magnetic resonance imaging (MRI), and fluorodeoxyglucose-positron emission tomography (FDG-PET) scans of these patients. RESULTS: Of the 10 patients with ictal hypersalivation, seven patients had nondominant/right TLE, and three patients had dominant/left TLE. All patients had hippocampal atrophy on volumetric MRI. Eight of the 10 patients underwent standard temporal lobectomy with amygdalohippocampectomy (six right, two left). All of the operated-on patients had a seizure-free (Engel class I) outcome, and their increased salivation resolved. Two patients, who did not undergo surgical treatment, continue to have complex partial seizures with increased salivation. CONCLUSIONS: We conclude that increased salivation as a prominent ictal finding in complex partial seizures of temporal lobe origin is more likely to be of nondominant temporal lobe origin. Further studies with larger numbers of patients are needed to replicate this finding.

Adult↗
PubMed1989

[Determination of insulin in saliva and its correlation with plasma insulin. Assessment of the possible participation++ of the salivary glands in the production of the hormone].

The finding of immunoreactive insulin (IRI) in saliva and an insulin-like protein, similar to pancreatic insulin and with the same biological activities, suggest that both products are pancreatic insulin stored and/or eliminated in the salival manner or an extrapancreatic hormone synthesis, bearing in mind the features which both glands share. The aim of this study is to ascertain whether the amount of insulin from saliva depends on plasmatic insulin and, if so, whether this is a form of elimination. Our results pointed out that the amount of insulin in saliva is similar to the plasmatic insulin in those patients with normal pancreatic function. The oral glucose tolerance test was carried out on 20 patients. The maximum insulin level was produced at the same time as maximum serum glucose level, taking place 60 minutes later. These data, support the concept that salival insulin is a product of the elimination more than synthesis by salival glands, however we can not exclude the possibility of synthesis by the salival gland without direct studies, the ideal test being the immunocytochemist.

C-Peptide↗
PubMed1992

Salivatory responses to classical and nontraditional parasympatholytic agents in human subjects: critical comments.

Both classical (atropine, scopolamine) and nontraditional (pirenzepine, telenzepine) cholinolytic agents themselves cause no salivation in human subjects. Ordinarily, they block salivation caused by pilocarpine. Conversely, they all stimulate intense salivatory response in the chronically denervated human parotid gland. The author presents critical comments on the concept that cholinolytic agents cause salivation by suppression of the mechanism of presynaptic autoinhibition. An alternative explanation of the initial cholinomimetic effect of cholinolytic agents is suggested.

Adolescent↗
PubMed1990

A comparison of the anticholinergic effects of two formulations of disopyramide in healthy volunteers.

Eight healthy male volunteers took a single oral dose of one of the following: Rythmodan (conventionally formulated disopyramide) 150 mg; Rythmodan 250 mg; Rythmodan Retard (controlled-release disopyramide) 250 mg; placebo. The subjects were allocated double-blind to sessions and treatments according to a Latin square design. In each session pupil diameter, heart rate, salivation, and QT interval were measured immediately before and at 1, 2, 3, 4, 6, 8, and 24 h after the drug. QT interval was corrected for heart rate (QT60). Plasma concentrations of total and unbound disopyramide were also determined at each time point. Both formulations of disopyramide reduced salivary output and increased QT60 interval, but there was not significant difference between the effects of the three active treatments. Neither formulation had any effect on pupil diameter or heart rate. The peak plasma concentration of unbound disopyramide was reached 2 h after Rythmodan and 4 h after Rythmodan Retard. The peak plasma concentration of disopyramide was significantly lower after Rythmodan Retard 250 mg than after Rythmodan 250 mg. The plasma concentration of unbound disopyramide was positively correlated with the reduction in salivation and prolongation of the QT60 interval. The reduction in salivation is likely to reflect blockade of muscarinic receptors by disopyramide, whereas the increase in QT60 interval is likely to be related to a direct effect of the drug on the heart. The results of this single-dose study do not indicate that disopyramide in the controlled-release formulation would be better tolerated by patients than conventionally formulated disopyramide.

Administration, Oral↗
PubMed1984

Differential response to cholinergic stimulation in psychogenitically selected rat lines.

Male and female rats of two lines psychogenetically selected for bipolar extremes in shuttle box avoidance were evaluated for tremor, salivation, chromodacryoorhea, and hypothermia following treatment with the muscarinic cholinergic agonist oxotremorine. Roman Low-Avoidance (RLA/Verh) rats exhibited more pronounced oxotremorine-induced tremor, chromodacryorrhea, and hypothermia than Roman High-Avoidance (RHA/Verh) rats. There was a sex difference only for a chromodacryorrhea response, with females exhibiting a greater response following oxotremorine than males. In a subsequent experiment using female rats of both rat lines, it was demonstrated that pre-treatment with the cholinergic antagonist scopolamine blocked oxotremorine-induced tremor, salivation and chromodacryorrhea responses in both rat lines and reduced the hypothermic effect observed in RLA/Verh rats (but not the much weaker hypothermia found in RHA/Verh rats) after oxotremorine injection. Pretreatment with the peripherally active cholinergic antagonist methscopolamine significantly reduced oxotremorine-induced salivation and chromocacryorrhea and somewhat decreased tremor and hypothermic responses in both rat lines. These results stand in contrast to the results of earlier research in which RHA/Verh rats exhibited greater behavioral depression in a tunnel maze than RLA/Verh rats following cholinergic manipulations. In view of evidence that these rat lines do not differ in number of muscarinic brain receptors, the present results may be due to genetic differences in other aspects of cholinergic neurotransmitter function, differences in the function of other neurochemical systems, or differences in the absorption, distribution, or metabolism of oxotremorine.

Animals↗
PubMed1984

Clonidine inhibits salivary secretion by activation of postsynaptic alpha 2-receptors.

The effects of clonidine on the submaxillary gland of the rat were studied. Doses ranging between 100 to 3.000 micrograms/kg produced a sustained secretory response which was blocked by 0.1 mg/kg of prazosin but not by 1 mg/kg of yohimbine. Clonidine 10 micrograms/kg markedly inhibited the salivation induced by noradrenaline, methacholine and substance P but not that induced by isoproterenol. The inhibition caused by the alpha 2-agonist was greater for noradrenaline than for either methacholine or substance P. Blockade of alpha 2 adrenoceptors with yohimbine (0.3 - 1 mg/kg) prevented the inhibition by clonidine of noradrenaline, methacholine and substance P induced salivation. On the other hand, prazosin 0.1 mg/kg did not modify the inhibition by clonidine of methacholine induced secretion. The results obtained indicate that clonidine exerts a dual effect on salivary secretion: at high doses it elicits salivation through activation of alpha 1-adrenoceptors; at the dose of 10 micrograms/kg clonidine activates alpha 2-adrenoceptors which inhibit the secretory response evoked through either muscarine, substance P and alpha 1-adrenoceptor agonists.

Animals↗
PubMed1986

Bronchial, cardiovascular and secretory responses after central administration of capsaicin in the guinea-pig.

Capsaicin was injected intracisternally (i.c.), intrathecally (i.th.) or intravenously (i.v.) into guinea-pigs anaesthetized with urethane and ventilated artificially. The effects of 0.2-100 micrograms capsaicin on insufflation pressure, heart rate, arterial blood pressure and salivation were recorded. Low i.c. doses of 0.2 and 2 micrograms capsaicin induced bradycardia, hypertension and salivation but no change in insufflation pressure. An insufflation pressure increase, i.e. bronchoconstriction, was observed with 20 or 100 micrograms capsaicin i.c. and this was associated with tachycardia and hypertension. Bronchoconstriction after 20 micrograms capsaicin i.c. was augmented by propranolol (1 mg/kg i.v.). It was, however, unaffected by bilateral cervical vagotomy and could also be induced by i.th. capsaicin injections in the lumbar region. Capsaicin (3 micrograms/kg) injected i.v. induced bronchoconstriction and tachycardia. Propranolol enhanced bronchoconstriction but did not reduce the tachycardia indicating that capsaicin led to activation of sympathetic bronchial but not cardiac fibers. These results also indicate that i.c. capsaicin caused reflex responses consisting of salivation, bronchodilatation bradycardia and hypertension. High doses injected i.c. or i.th. also caused tachycardia and bronchoconstriction. This latter effect, however, was neither a vagal reflex nor did it seem to result from activation of central terminals of afferent fibers with subsequent release of mediators from the peripheral endings due to antidromic spread of nerve impulses. Instead, capsaicin seemed to be readily resorbed into the systemic circulation and thus acting at peripheral endings to cause bronchoconstriction and tachycardia.

Airway Resistance↗
PubMed1988

Effects of a controlled-release formulation of trazodone on psychomotor and autonomic functions in healthy volunteers: comparison with trazodone (conventional formulation), amitriptyline and placebo.

Eight healthy male volunteers participated in four experimental sessions. In each session the subjects ingested a single dose of one of the following drugs: trazodone (controlled-release formulation), trazodone (conventional formulation), amitriptyline and placebo. Both trazodone and amitriptyline reduced subjectively rated alertness and increased digit cancellation time, and amitriptyline also reduced critical flicker fusion frequency. Both antidepressants reduced salivation, trazodone also caused miosis. There were no consistent differences between the effects of the two formulations of trazodone. The results of the psychological tests are indicative of the sedative properties of the antidepressants. It is likely that the reduction in salivation and pupil diameter by trazodone reflect alpha-adrenoceptor blockade, whereas the reduction in salivation by amitriptyline may be due to both cholinoceptor and alpha-adrenoceptor blockade.

Administration, Oral↗
PubMed1997

Comparison of the effects of high ambient temperature and clonidine on autonomic functions in man.

The effects of two interventions, high ambient temperature, a sympathetic activator, and clonidine, a centrally acting sympatholytic drug, were compared on a number of autonomic functions. Eight healthy male volunteers participated in four weekly sessions. Each session was associated with one of the following treatments: placebo (physiological saline infused intravenously over 10 min) at 20 degrees C; clonidine hydrochloride (1.5 micrograms kg-1 in 10 ml infused intravenously over 10 min) at 20 degrees C; placebo at 40 degrees C; clonidine at 40 degrees C. Subjects were allocated to treatments and sessions according to a double-blind (for drug condition) balanced design. In each session, the following indices of autonomic function were recorded: systolic and diastolic blood pressure, heart rate, salivation, body temperature, plasma noradrenaline and adrenaline concentrations, baseline and carbachol-evoked sweating, physiological finger tremor. Raised ambient temperature (40 degrees C) caused increases in heart rate, body temperature, carbachol-evoked sweating and physiological finger tremor. Clonidine (at 20 degrees C) reduced systolic blood pressure, body temperature, salivation and plasma noradrenaline concentration, but did not affect any of the other measures. Clonidine (at 40 degrees C) counteracted the increase in heart rate, but not the increases in carbachol-evoked sweating and finger tremor, evoked by high ambient temperature. The high ambient temperature condition abolished the body-temperature-lowering effect of clonidine, but did not modify the effects of clonidine on systolic blood pressure, salivation and plasma noradrenaline concentration. These result indicate that while the effects of the heat stressor are consistent with an increase in sympathetic activity, and most of the effects of clonidine are consistent with a decrease in sympathetic activity, only two functions (body temperature and heart rate) were affected in opposite directions by the two interventions. Indeed physiological antagonism between the two interventions could be demonstrated on body temperature and heart rate only, and there was no evidence for an interaction between the effects of the two variables on any of the other indices of autonomic activity. The failure of clonidine to affect two sympathetically mediated functions, carbachol-evoked sweating and physiological finger tremor, under either temperature condition, indicates that central alpha 2-adrenoceptors cannot be involved in the regulation of these functions.

Adrenergic alpha-Agonists↗
PubMed1981

Potentiation by spiperone and other butyrophenones of fluid secretion by isolated salivary glands of ixodid ticks.

Isolated salivary glands from the ixodid tick, Amblyomma hebraeum Koch are stimulated to secrete fluid when exposed to dopamine (DA), the maximum response occurring at 10(-6) M. Spiperone, and a number of other butyrophenone derivatives, although lacking intrinsic activity, are able to potentiate the secretion elicited by supramaximal concentrations of DA; this potentiation by spiperone is evident at concentrations in the femtomolar range. Tranylcypromine, a potent, competitive inhibitor of monoamine oxidase (MAO) in tick salivary gland homogenates, has both intrinsic activity and potentiates DA-induced salivation. The fact that spiperone potentiates ergometrine-induced salivation that the prime mechanism of the butyrophenone effect is not by inhibiting catecholamine catabolism. The results also suggest that the receptor for DA and that for butyrophenones are distinct sites. Droperidol, benperidol and bromperidol, all potent neuroleptic drugs, failed (at 10(-9) M) to potentiate salivation. By contrast, R951, R27275 and R1187 (all at 10(-9) M) were very effective potentiators on the salivary gland system, despite the fact that they lack the basic structural requirements for neuroleptic activity. These results suggest that the butyrophenone site in tick salivary glands is different from butyrophenone binding sites in mammalian CNS.

Animals↗
PubMed1992

Abstinence from smoking decreases habituation to food cues.

Smokers typically gain weight after cessation due, in part, to increased caloric intake. This increase may be due to enhanced responding to sensory characteristics of foods resulting from a failure to habituate to food cues. To test this possibility, salivation to eight presentations of strawberry yogurt was assessed in male smokers and nonsmokers in two sessions. To test stimulus specificity, on the ninth trial, subjects were presented either more strawberry yogurt or lemon yogurt. Smokers were studied under nonabstinent or abstinent conditions. Salivation for nonabstinent smokers and nonsmokers decreased over presentations, while abstinent smokers showed little change. Nonabstinent smokers and nonsmokers recovered salivation when the new flavor yogurt was presented, and showed greater consumption on the final trial for the different versus same flavor yogurt. Nonabstinent smokers participated in additional within-session smoking sessions to control for withdrawal. Nonabstinent subjects were not different across smoking or not smoking sessions, suggesting the effects are not due to the acute effects of withdrawal.

Adolescent↗
PubMed1996

Kallikrein and salivary secretion in rats during heat exposure.

RP 67850, a NK1 receptor antagonist, inhibited the sialogogic effect of Substance P (SP). Heat-induced salivation was indirectly measured through the changes in body weight. Thermolytic salivation was reduced by atropine and RP 67580 and thus would be mainly controlled by acetylcholine and tachykinins. This salivation was associated with a large depletion of kallikrein in submaxillary glands. This depletion was not inhibited by atropine and RP 67580. Feeding has been reported to reduce amylase activity in parotid glands but did not modify the kallikrein content in submaxillary glands. Heat exposure did not modify amylase activity. There is a dissociation between the releases of amylase and kallikrein from salivary glands.

Animals↗
PubMed1982

Use of substance P fragments to differentiate substance P receptors of different tissues.

The C- and N-terminal fragments of substance P were compared to the parent molecule with respect to their ability to: (a) contract the isolated guinea pig ileum, (b) induce salivation in the rat, (c) excite single cat dorsal horn neurones, and (d) induce scratching by intracranial injections in mice. C-terminal fragments as small as the heptapeptide were potent SP agonists on all assay systems. C-terminal fragments containing five amino acids or less were, at most, only weakly active. The C-terminal hexapeptide was a potent SP receptor stimulant on the isolated guinea pig ileum and, when directly applied by microiontophoresis, on cat dorsal horn neurons. However, the same compound was only 2-5% as potent as substance P in eliciting salivation and scratching in vivo, an indication that this fragment may be especially labile to enzymatic degradation. N-terminal fragments were totally inactive on the isolated guinea pig ileum. On the rat salivation and central nervous system assays, however, N-terminal fragments were capable of weak SP-like activity. It is concluded that SP receptors exist in multiple forms which we have labelled SP1 and SP2 receptors for those insensitive or sensitive to N-terminal fragments, respectively.

Animals↗