[The effect of changes in the intraoral environment on the state of the periodontium in rats. I. Loss of salivation and increased salivation].
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Measurement of tachykinin-induced salivation in conscious rats.
A method of quantitatively measuring tachykinin-induced salivation in conscious, male, Sprague-Dawley rats is described. Salivation is quantified by determining the weight of a preweighed, absorbant foam cube after it has been used to swab the oral cavity of a tachykinin challenged rat. Salivation is induced by intravenous (i.v.) injection of sialogogues (microgram/kg) via the lateral tail vein. Measurements are made immediately after injection. Substance P (Sub.P), Sar9, Met (O2) 11Substance P (Sar9 Sub.P), a selective neurokinin (NK) 1 receptor agonist, Physalaemin and Eledoisin are equipotent sialogogues as determined by this method. Neurokinin A (NKA), the endogenous NK2 receptor agonist, is 0.27 (0.14-0.46) times as potent as Sub. P, while (Suc-[Asp6, MePhe8]Substance P(6-11), (senktide), a selective NK3 receptor agonist, only induced salivation at 300 microgram/kg. Acetylcholine (Ach) is only 0.006 (0.002-0.012) times as potent as Sub.P. Treatment with the neurokinin antagonist [D-Arg1, D-Trp7,9 Leu11]-Substance P (spantide) dose-dependently inhibits Sub. P stimulated salivation. Atropine dose-dependently inhibits Ach induced salivation but is inactive against Sub.P-induced salivation. These data are consistent with literature values and indicate that this method provides a simple, quantitative model, free of any possible anesthetic side effects, for the measurement of neurokinin stimulated salivation and the assessment of potential neurokinin antagonists in vivo.
Acetylcholine↗
Antagonism of conditioned salivation in conscious dogs by antihypertensive drugs.
Methyldopate (methyldopa (ethyl ester)), carbidopa, clonidine, and ST-91 were evaluated for their effects on conditioned salivation in unanesthetized dogs. Clonidine produced dose-dependent inhibition of salivation 20 min after an intravenous injection. At equivalent and larger doses, ST-91, a clonidine analog which does not penetrate the blood-brain barrier, was ineffective in inhibiting conditioned salivation, suggesting that central rather than peripheral mechanisms are involved in clonidine-induced inhibition of salivation. Methyldopate also produced a dose-dependent inhibition of salivation in dogs. The mechanism involved in methyldopa-induced inhibition of salivation may involve both central and peripheral mechanisms because carbidopa, an inhibitor (like methyldopa) of peripheral aromatic decarboxylase (EC 4.1.1.28), significantly inhibited salivation.
Animals↗
Salivation discordant with hunger.
In the present study, the authors tested whether an increase in salivation is associated with an increase in subjectively experienced hunger. After conditioning, subjects showed a significant increase in salivation flow. Hunger levels, however, were significantly decreased after conditioning. No correlation was found between salivation flow and hunger levels. It is argued that salivation responses and subjectively experienced hunger are loosely coupled systems. Salivation flow reflects the learning history of a subject which may sometimes be paralleled by a biological state which is called hunger, whereas, at other times, hunger may be absent. The authors conclude that conditioning of preparatory responses such as salivation depends on the probability relationship between exposure to cues (CSs) and food intake (US), as well as the intensity of the US.
Adult↗
The mechanism of the clonidine-induced reduction in peripheral parasympathetic submaxillary salivation.
The mechanism of the clonidine induced reduction in submaxillary salivation evoked by electrical stimulation of the chorda tympani was investigated in anaesthetised cats. This effect of clonidine was found to be dose and frequency dependent. In addition to clonidine, tramazoline, also a preferential presynaptic alpha-adrenoceptor agonist, produced a reduction in electricallly evoked salivation. Methoxamine, noradrenaline and naphazoline, which are less potent presynaptic alpha-receptor agonists, caused increases in salivation. Phentolamine only partially antagonized the decrease in salivation produced by clonidine whereas it was virtually abolished by yohimbine. Clonidine increased salivation evoked by intra-arterial injections of carbachol. These findings suggest that clonidine reduces peripheral parasympathetically evoked submaxillary salivation by activation of presynaptic alpha-adrenoceptors which inhibit cholinergic transmission.
Adrenergic alpha-Agonists↗
Effect of food change on consumption, hedonics, and salivation.
This study assessed the influence of introducing a new food after repeated presentations of one food on food consumption, hedonics, and salivation. Male subjects were provided repeated 150-calorie courses of pizza or cheeseburger until satiety. Hedonics and salivation were measured before each course. Subject were then provided an additional 450 calorie course of the same or the new food. During the development of satiety, subjects showed reliable increases in fullness and decreases in hunger and hedonics. Salivation briefly increased to maximal salivation, followed by reliable decreases. No differences in pattern of change for fullness, hunger, hedonics or salivation were noted across foods. Presentation of the new food resulted in significantly greater caloric consumption than another serving of the same food (130 vs. 44.5 kcal), an increase in hedonics and salivation relative to presentation of the same food, with no influence on hunger or fullness. These results suggest that after satiety develops, response recovery for subjective, physiological, and behavioral components of eating can be observed when new, palatable foods are presented.
Adolescent↗
Autonomic mechanisms underlying capsaicin induced oral sensations and salivation in man.
The effects of capsaicin, citric acid and nicotine applied to the apex or radix of the tongue on taste sensations and salivation were studied in relation to the presence of substance P immunoreactive neurones in man. Application of capsaicin (30 micron) to the apex of the tongue or to the palatinal mucosa, but not to the radix of the tongue, caused a reproducible burning sensation and salivation from the submandibular-sublingual and parotid glands. The salivation response to capsaicin was reduced by methylscopolamine pretreatment. Similar levels of substance P immunoreactivity were present in the lingual apex and radix area (including vallate papillae) of man, while in the cat about 4 times higher levels of substance P immunoreactivity were present in the vallate papillae than in the lingual apex. Immunohistochemistry showed that in the cat many substance P immunoreactive nerves were associated with the taste buds of the vallate papillae, while in man substance P immunoreactive fibres were only seen penetrating into the epithelium of the lingual apex. In addition some subepithelial blood vessels in all regions were surrounded by substance P immunoreactive nerves in both cat and man. Citric acid application to the tongue apex caused both submandibular-sublingual and parotid salivary secretion concomitant with a burning sensation. Salivary secretion was also seen after citric acid application to the radix of the tongue. This response was associated with a sour taste. The salivation response to citric acid was not significantly reduced by methylscopolamine pretreatment. Lingual apex application of nicotine was associated with a sweet taste and a small rise in salivary secretion rate. This response was not significantly reduced by methylscopolamine. In conclusion, the sensitivity to capsaicin of the human tongue is restricted to the apex portion. This is in parallel with the occurrence of intraepithelial substance P immunoreactive nerve fibres. Capsaicin induced salivary secretion seems mainly to be mediated via parasympathetic, cholinergic reflex mechanisms. Citric acid and nicotine induced salivation responses are comparatively more resistant to methylscopolamine pretreatment.
Adolescent↗
Inter-organ relation between salivary gland and kidney in lithium excretion. II. Salivary, renal and systemic clearances of lithium under continuous stimulation of salivation in water loaded dogs.
This study was undertaken to investigate the effects of water loading on lithium clearance in dogs under the continuous stimulation of salivation as well as to clarify the mechanism of the inter-organ relation between salivary gland and kidney in lithium excretion. Dogs were given intravenously 0.145 meq/kg of lithium chloride followed by the continuous stimulation of salivation with citric acid solution. Fifty ml of water was loaded orally 7 times at 1-h intervals. Parotid and mandibular-sublingual salivas were collected separately by means of permanent fistulae. (1) Plasma concentrations of lithium were not significantly different from either those in the experiment with continuous stimulation under no water loading or those in the control experiment without continuous stimulation. (2) Salivary clearance of lithium was markedly increased compared with that in the control experiment. The urinary flow rate, which was decreased under the continuous stimulation of salivation without water loading, was restored by the water loading. The renal clearance of lithium, which was also decreased under the continuous stimulation, remained at the reduced level under the condition of this study. Consequently, the systemic clearance of lithium did not change from that in the experiment under the continuous stimulation without water loading or that in the control experiment. (3) It was suggested that the salivary and renal excretion mechanisms of lithium might be similar to those of potassium, since a similar interrelation between salivary and renal clearances was observed for potassium. (4) It was suggested that the reduction in the renal clearance of lithium under the continuous stimulation of salivation was attributed to the sodium loss caused by the excessive salivation.
Animals↗
The effect of clonidine on centrally and peripherally evoked submaxillary salivation.
In anaesthetised cats, clonidine (10 microgram/kg, i.v.) produced a 60% reduction in submaxillary salivation induced by brain stem stimulation at 10 and 15 Hz and reductions of 35 and 15% in salivation evoked by chorda tympani nerve stimulation at 5 and 15 Hz respectively. Pretreatment with clonidine (20 microgram/kg/day, orally) for 28 days reduced peripherally evoked salivation by 45%. These results suggest that both central and peripheral mechanisms are involved in the diminished salivation produced by clonidine, and the reduction on peripheral stimulation may reflect the presence of presynaptic alpha-adrenoceptors inhibiting cholinergic transmission.
Animals↗
gamma-Preprotachykinin-(72-92)-peptide amide potentiates substance P-induced salivation.
The effects of gamma-preprotachykinin-(72-92)-peptide amide [gamma-PPT-(72-92)-NH2] on salivation in the rat were investigated and were compared with salivation responses elicited by a variety of other tachykinin and related peptides. On intravenous injection or continuous infusion, gamma-PPT-(72-92)-NH2, a naturally occurring N-terminally extended derivative of neurokinin A (NKA), potently stimulated salivation. The rank order of potency of peptides that stimulated salivation was: NPK greater than gamma-PPT-(72-92)-NH2 greater than substance P greater than NKA = Asp-Ala-NKA. Moreover, gamma-PPT-(72-92)-NH2, like NPK, potentiated the effects of substance P on salivary secretion. These results indicate that the actions of gamma-PPT-(72-92)-NH2 may be pharmacologically or physiologically relevant in the actions of tachykinin peptides.
Amino Acid Sequence↗
Action of clonidine on centrally evoked salivation in anaesthetized cats.
1. Clonidine (4 microgram/kg) given intracisternally to anaesthetized cats inhibited brain stem-evoked parasympathetic submaxillary or parotid salivation by 62% at 5 Hz and 44% at 15 Hz. 2. The inhibitory action of clonidine on salivation was equally prevented by pretreatment with either intracisternal yohimbine (175 microgram/kg) or phentolamine (250 microgram/kg), used as preferential pre- and post-synaptic alpha-adrenoreceptor-blocking drugs respectively. 3. the inhibition of centrally evoked salivation by clonidine is due to an action on alpha-adrenoreceptors but no clear evidence was obtained to indicate whether these were located pre- or post-synaptically. This is in contrast to the preferential presynaptic action of clonidine in reducing peripheral parasympathetic nerve-evoked salivation.
Animals↗
Studies on tachykinin (neurokinin) receptor coupled with inositol phospholipid hydrolysis and salivation in rat salivary glands.
3H-substance P binding to the membranes of rat salivary glands was studied. The Kd and Bmax values were found to be 0.34 nM and 141 fmole/mg protein respectively using established natural occurring tachykinins to displace the binding. The rank order of potency was identified as substance P > neurokinin A > neurokinin B. These natural occurring tachykinins stimulate inositol phospholipid hydrolysis in slices of rat salivary glands, and the rank order of potency was also substance P > neurokinin A > neurokinin B. When salivation was induced by natural occurring tachykinins and acetylcholine (via i.v. route) in anesthetized rats with doses eliciting equivalent salivating responses, atropine blocks acetylcholine- as well as neurokinin B-, but not substance P- or neurokinin A-induced salivation. Based on the results mentioned above, we make a tentative conclusion that multiple receptor subtypes of neurokinins may exist in rat salivary glands. The neurokinins B receptor subtype is likely located presynaptically in the cholinergic nerve endings, whereas substance P and/or neurokinin A receptor subtypes may exist in the glandular tissue. The salivation induced by these neurokinins is likely through the activation of receptors, which are coupled to phosphatidylinositol turnover pathway.
Acetylcholine↗
Short-term effects of energy density on salivation, hunger and appetite in obese subjects.
Obese patients were admitted to a metabolic unit for weight loss. On two paired-test days subjects were given disguised preloads of 100 kcal (0.42MJ) or 300 kcal (1.26MJ). When presented with a meal one hour after the preload, subjects salivated more and reported more hunger, but not appetite, after the low compared to the high preload. A different group of 14 subjects were given preloads of the same energy content (200 kcal, 0.84MJ) on paired-test days. On one day they took 1 g methyl cellulose with 100 ml water drink immediately before the preload. Neither the energy-dilution effect of the water, nor the effect of the methyl cellulose caused a significant decrease in salivation, hunger or appetite scores one hour after the preloads of equal energy content. These results show that salivation and hunger are inversely related to short-term changes in energy intake in obese subjects. Alterations in energy density without changing energy intake or the ingestion of methyl cellulose have no effect on salivation, hunger or appetite.
Adolescent↗
Effect of a novel tachykinin, substance K, on salivation in rats.
A study of the effects of substance K (SK) and its synthetic fragments on salivation was performed. The rank order of potency of tachykinins that elicited salivation was as follows: physalaemin greater than substance P greater than eledoisin greater than kassinin greater than Arg-SK-(1-10) greater than SK-(1-10) greater than SK-(3-10). SK-(6-10) showed no activity. Atropine (1 mg/kg i.v.) had no effect on SK-induced salivation.
Amino Acid Sequence↗
Breakdown of dietary restraint following mere exposure to food stimuli: interrelationships between restraint, hunger, salivation, and food intake.
It was hypothesised that the hunger-enhancing effects of exposure to the sight and smell of palatable food would disinhibit eating in restrained eaters (self-reported dieters). In two experiments exposure to palatable food stimuli led to increases in motivational (hunger) ratings and salivation, and was followed by overeating in restrained subjects compared with the control condition (no food during exposure) and a condition in which nonpreferred food was presented during the exposure phase. The food intake of unrestrained subjects, on the other hand, was reduced following exposure to palatable food in the first experiment. This shows that breakdown of dietary restraint can be induced by food stimuli even when the food does not constitute a preload. Mere exposure to the sight and smell of palatable food is sufficient to precipitate loss of dieting motivation. The effects of exposure on hunger and salivation were, in general, unrelated to food intake or degree of dietary restraint. Therefore, changes in hunger do not appear to directly mediate increased food intake in dieters. Instead, it is tentatively suggested that anxiety resulting from exposure to liked food may play a role both in disinhibiting eating and suppressing salivation in restrained subjects.
Adolescent↗
Thermal salivation in rats, anesthetized with barbiturates, chloralose, urethane and ketamine.
1. The relationship between thermal salivation (TS) and thermoregulation was studied in anesthetized rats. 2. Of the 6 anesthetics used, ketamine-anesthetized rats secreted the largest amount of saliva. Salivation, however, was thermal and not induced by ketamine itself. 3. Ketamine-anesthetized rats readily secreted saliva at core temperatures less than 40 degrees C but TS was remarkably enhanced by hyperthermia of 40-42.5 degrees C. 4. The equilibrium phase in the triphasic heat response of core temperature was a consequence of equilibrium between heat gain and heat loss by salivation.
Anesthetics↗
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↗
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↗