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At least 217 records · Page 12Linked to original sources
PubMed1979

Assessment of the effects of vasoactive intestinal peptide (VIP) on blood flow through and salivation of the dog salivary gland in comparison with those of secretin, glucagon and acetylcholine.

1. The vascular bed of the submandibular gland in situ was perfused with blood through the glandular artery at a constant pressure in anesthetized dogs. All drugs were administered intra-arterially. 2. Vasoactive intestinal peptide (VIP), secretin and acetylcholine produced a dose-dependent increase in blood flow through the artery (vasodilatation) but glucagon was almost ineffective. 3. Dose-blood flow response curves for VIP and secretin were parallel, and VIP was about 100 times as potent as secretin on a molar basis. Dose-blood flow response curves for acetylcholine were flatter than those for VIP and secretin. Acetylcholine was approximately as potent as secretin on a molar basis. 4. No tachyphylaxis developed to the vasodilator action of VIP. 5. The vasodilator responses to VIP and to electrical stimulation of the chordolingual nerve were scarcely modified by (-)-hyoscyamine in doses that fully antagonized the vasodilator response to acetylcholine. 6. VIP, secretin and glucagon were ineffective in eliciting salivary secretion. 7. The possibility that VIP is released from parasympathetic vasodilator nerves and mediates the atropine-resistant vasodilatation in the dog submandibular gland is discussed.

Acetylcholine↗
PubMed1988

Tachykinin involvement in parasympathetic nerve-evoked salivation of the ferret.

1. The tachykinin antagonist (D-Arg1, D-Cl2Phe5, Asn6, D-Trp7.9, Nle11)-substance P, injected intravenously, blocked salivary secretion from the ferret parotid and submandibular glands in response to subsequent i.v. injections of the tachykinins, substance P and neurokinin A. 2. The tachykinin antagonist reduced the parasympathetic nerve-evoked secretion of parotid and submandibular saliva by 15-20% and 35-40%, respectively. Atropine abolished the remaining secretory response. 3. The 'atropine-resistant' parasympathetic nerve-evoked secretion of saliva from the parotid and submandibular glands (about 5 and 30%, respectively, of that before administration of atropine) was abolished by the tachykinin antagonist. 4. The tachykinin antagonist was without effect on the protein concentration of parotid and submandibular saliva secreted in response to parasympathetic nerve stimulation. Parotid and submandibular saliva lacked amylase. 5. Atropine reduced the protein concentration of the submandibular saliva secreted in response to parasympathetic nerve stimulation by 50%; this was the protein concentration of substance P-evoked saliva. 6. The secretory response to methacholine and to stimulation of preganglionic sympathetic nerve fibres, tested in rats, was unaffected by the tachykinin antagonist, contra-indicating an unspecific action of the antagonist. 7. The results suggest that the neuronal release of tachykinins is probably important in the nerve-evoked secretory response of the parotid and submandibular glands.

Amylases↗
PubMed1989

Effects of yohimbine on submaxillary salivation in dogs.

1. The effects of yohimbine (0.5 mg kg-1 i.v.) on both resting and parasympathetic and sympathetic stimulation-induced submaxillary salivary responses were investigated in the anaesthetized dog. 2. Salivary secretion was increased significantly for a period of 45 min following an injection of yohimbine. 3. Sectioning of the chorda tympani (but not the cervical sympathetic) nerve abolished the yohimbine-induced increase in resting salivary secretion and potentiated that elicited by electrical stimulation of the chorda tympani nerve. 4. These results show that yohimbine increases submaxillary secretion by inhibition of presynaptic alpha 2-adrenoceptors located on the chorda tympani, which inhibit cholinergic transmission.

Anesthesia↗
PubMed1966

A study of parotid salivation in the horse.

1. Saliva flowed from the horse's parotid duct only during mastication.2. The surface-active local anaesthetic administered by mouth inhibited salivary secretion.3. Salivary secretion was stimulated by pilocarpine and inhibited by atropine.4. The volume and composition of saliva secreted in 24 hr from one parotid duct was determined.5. The concentration of sodium, potassium, calcium, chloride and bicarbonate depended upon the rate of flow. The highest concentrations of these electrolytes were observed during periods of high flow rates.6. Horse parotid saliva contained a high concentration of calcium.7. In the absence of a dietary supplement of sodium bicarbonate, the sodium concentration of the saliva fell after about 21 days. There was an associated increase in the potassium concentration. The addition of a sodium supplement restored the sodium concentration of the saliva within 24 hr.

Animals↗
PubMed1994

Parasympathetic-mediated reflex salivation and vasodilatation in the cat submandibular gland.

The aim of the present study was to compare and characterize the secretory and vasodilator effects induced by chorda lingual nerve (CLN) stimulation (i.e., direct parasympathetic stimulation) and reflex parasympathetic stimulation in the submandibular gland (SMG) of sympathectomized cats. The increase in blood flow and salivary secretion in response to electrical stimulation of the central cut ends of the vagus and inferior alveolar nerves, as well as to stimulation of the CLN at a site approximately 5 mm distal to the intersection of the CLN and the SMG duct (site D) was completely abolished by section of the chorda tympani nerve (CTN). Neither response to CLN stimulation at a site nearly 5 mm proximal to the intersection of the CLN and the SMG duct (site C) was affected by CTN section. Section of the CLN at a site approximately 5 mm distal to the intersection of the CTN and the CLN abolished the submandibular salivary and vasodilator responses elicited by CLN stimulation at site D but had no effect on the two responses evoked by CLN stimulation at site C. The blood flow increases evoked by electrical stimulation of the CLN at site D were greatly reduced by prior treatment with the autonomic ganglion blocker hexamethonium, but the vasodilator responses evoked from site C were reduced much less. These data suggest that the secretory and vasodilator responses elicited by CLN stimulation at site D and those by vagus and inferior alveolar nerve stimulation are mediated largely via a parasympathetic reflex mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The effect of sucrose and fat in cookies on salivation and oral retention in humans.

Six adults were served accurately weighed portions (about 5 g) of cookies varying in sucrose and fat content. The cookies were chewed and spat out at the time the subjects were ready to swallow. Additional spittings were collected at intervals up to two, three, and four min. Chewing time decreased with increase in sucrose, or with increase in fat. The volume of saliva in each spitting was calculated from its wet and dry weights, and it was assumed either (a) that saliva produced during chewing was not carried over in the retained food, or (b) that saliva was incorporated in the retained food in the same proportion as in the first spitting. Both approaches revealed that salivary flow rates were independent of cookie formulation, with two exceptions: (1) The cookie highest in sucrose produced a significantly higher flow rate during chewing, and (2) the fat-free cookie, which was hard to chew, elicited an elevated flow rate up to two min. The total volume of saliva for the entire experimental period was similar for all formulations, except the latter. Masticatory effects, therefore, appeared to predominate over sweetness stimulation, unless sugar content was very high. The volume of saliva in the food bolus at the time of swallowing correlated with chewing time. Oral clearance of the cookies did not give straight lines when logarithms of retained material were plotted against time. Initial clearance rates appeared to diminish with increasing sucrose and fat content of the cookies. Effects of sugar and fat on all parameters may reflect changes in cookie texture and the sizes of particles produced within the mouth.

Adult↗
PubMed1998

Botulinum toxin decreases salivation from canine submandibular glands.

The objective of this study was to determine whether botulinum toxin types A and D reduced the production of saliva from the submandibular glands of 18 dogs. The left submandibular glands of 8 dogs were injected with increasing doses of botulinum type A toxin (range 10 to 70 units), and the left glands of 10 dogs were injected with botulinum type D toxin (50 or 100 units). The right gland of each dog was injected with equivalent volumes of saline solution to serve as control. Six days after the injection, the lingual nerve was electrically stimulated for 10 minutes (3 mAmp, 20 Hz). The resulting volume of saliva was collected and weighed. Overall, the glands injected with types A or D toxin produced significantly less saliva than comparable glands injected with saline solution. Six of 8 dogs injected with type A toxin showed a significant decrease in saliva production (range 10.1% to 19.2%, one-sided p value = 0.0375) when compared with the controls. Nine of 10 dogs injected with type D toxin demonstrated a highly significant reduction in saliva production (total average decrease = 60%, two-sided pvalue = 0.001) when compared with the controls. We concluded that intraglandular injections of botulinum toxin types A and D significantly reduced the production of saliva from canine submandibular glands. The potential applications of intraglandular injections of botulinum toxin are discussed.

Animals↗
PubMed2006

Pilocarpine-induced salivation and thirst in conscious rats.

The muscarinic receptor agonist pilocarpine is widely used as a sialogogue. It has been well-established that it also induces water intake in animals. However, the mechanisms underlying the relationships between these events are unknown. To address this problem, we examined water intake and parotid salivary secretion in conscious rats. Intraperitoneally injected pilocarpine increased both water intake and salivary secretion. Intracerebroventricularly injected pilocarpine also induced water intake, but not salivary secretion. Intracerebroventricularly applied atropine, a muscarinic receptor antagonist, suppressed the water intake produced by pilocarpine applied intraperitoneally and intracerebroventricularly. However, it did not affect the salivary secretion induced by pilocarpine applied peripherally. We conclude that peripherally applied pilocarpine affects the parotid glands and the thirst center in the central nervous system, while it may induce salivary secretion mainly via peripheral responses, but water intake mainly via the central nervous system.

Animals↗