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PubMed1965

Salivation.

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Dentistry↗
PubMed1987

Iatrogenic causes of salivary gland dysfunction.

Saliva is important for maintaining oral health and function. There are instances when medical therapy is intended to decrease salivary flow, such as during general anesthesia, but most instances of iatrogenic salivary gland dysfunction represent untoward or unavoidable side-effects. The clinical expression of the salivary dysfunction can range from very minor transient alteration in saliva flow to a total loss of salivary function. The most common forms of therapy that interfere with salivation are drug therapies, cancer therapies (radiation or chemotherapy), and surgical therapy. These therapies can affect salivation by a number of different mechanisms that include: disruption of autonomic nerve function related to salivation, interference with acinar or ductal cell functions related to salivation, cytotoxicity, indirect effects (vasoconstriction/dilation, fluid and electrolyte balance, etc.), and physical trauma to salivary glands and nerves. A wide variety of drugs is capable of increasing or decreasing salivary flow by mimicking autonomic nervous system actions or by directly acting on cellular processes necessary for salivation: drugs can also indirectly affect salivation by altering fluid and electrolyte balance or by affecting blood flow to the glands. Ionizing radiation can cause permanent damage to salivary glands, damage that is manifest as acinar cell destruction with subsequent atrophy and fibrosis of the glands. Cancer chemotherapy can cause changes in salivation, but the changes are usually much less severe and only transient. Finally, surgical and traumatic injuries interfere with salivation because of either disruption of gland innervation or gross physical damage (or removal) of glandular tissue (including ducts).

Bone Marrow Transplantation↗
PubMed1994

The vasodilator and secretory effects elicited by sympathetic nerve stimulation in cat submandibular gland.

The effects of electrical stimulation of the peripheral cut ends of the ascending cervical sympathetic trunk on vasomotor, particularly vasodilator, response were studied in relation to salivary secretion in the cat submandibular gland. The vasodilator and salivary responses were compared by stimulating the peripheral cut ends of the sympathetic nerve at various intensities (1-8 V), durations (5-60 s) and frequencies (1-100 Hz) using a 2 ms pulse duration. Electrical stimulation of the cervical sympathetic nerves caused vasoconstriction followed by vasodilatation and salivation. There were certain differences in the maximal responses of vasodilatation and salivation during sympathetic stimulation. For example, optimal frequencies for vasodilatation and salivation were 10 Hz and 20 Hz, respectively. Time-dependent increases in vasodilatation and salivary secretion were seen for periods of up to 30 s and 60 s, respectively. The volume of salivation was not necessarily correlated with the magnitude of vasodilator response. Prior treatment with an alpha-adrenoceptor blocking agent phentolamine largely reduced vasoconstriction (P < 0.01) and almost completely abolished salivary secretion (P < 0.01), but had only a slight inhibitory effect on vasodilatation (0.1 < P < 0.05). Propranolol (a beta-adrenoceptor blocking agent) pretreatment significantly decreased vasodilatation (P < 0.05) but had no statistically significant effect on vasoconstriction or salivation. Scopolamine (a muscarinic cholinoceptor blocking agent) had no effect on the responses followed by sympathetic nerve stimulation but abolished the vagal mediated reflex salivation, indicating that the salivation, but not vasodilatation, elicited by activation of the afferent fibers of the vagus nerve is mediated via parasympathetic muscarinic fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗
PubMed2006

Damage of the medial preoptic area impairs peripheral pilocarpine-induced salivary secretion.

The existence of neural connections between the medial preoptic area (MPOA) and the salivary glands and the increase in salivation by thermal or electrical stimulation of the MPOA have suggested an important role of MPOA in the control of salivary gland function. Although direct cholinergic activation of the salivary glands induces salivation, recent studies have suggested that salivation produced by i.p. pilocarpine may also depend on the activation of central mechanisms. Therefore, in the present study, we investigated the effects of bilateral electrolytic lesions of the MPOA on the salivation induced by i.p. pilocarpine. Adult male Holtzman rats (n = 11-12/group) with bilateral sham or electrolytic lesions of the MPOA were used. One, five, and fifteen days after the brain surgery, under ketamine anesthesia, the salivation was induced by i.p. pilocarpine (1 mg/kg of body weight), and saliva was collected using pre-weighed small cotton balls inserted into the animal's mouth. Pilocarpine-induced salivation was reduced 1 and 5 days after MPOA lesion (341 +/- 41 and 310 +/- 35 mg/7 min, respectively, vs. sham lesions: 428 +/- 32 and 495 +/- 36 mg/7 min, respectively), but it was fully recovered at the 15th day post-lesion (561 +/- 49 vs. sham lesion: 618 +/- 27 mg/7 min). Lesions of the MPOA did not affect baseline non-stimulated salivary secretion. The results confirm the importance of MPOA in the control of salivation and suggest that its integrity is necessary for the full sialogogue effect of pilocarpine. However, alternative mechanisms probably involving other central nuclei can replace MPOA function in chronically lesioned rats allowing the complete recovery of the effects of pilocarpine.

Animals↗
PubMed2000

Structure-activity relationships of sialogogic heptapeptides analogous to physalaemin.

OBJECTIVES: The rationale behind this study was to determine in detail which amino acids in physalaemin are crucial to its sialogogue activity, with a view of synthesizing new sialogogues which might be of use in the treatment of dry mouth. METHODS: With the progressive elimination of amino acids, one by one, from the C- and N-terminal regions, 126 heptapeptides were newly synthesized by the multipin peptide method, for comparison with II naturally occurring tachykinins. RESULTS: The C-terminal amide in position II was essential for salivation, but not the pyrolidine group or the N-terminal amino acid residues in positions I to 4. In 18 heptapeptides in which M in position II (MII) was replaced by another amino acid, one by one, none caused salivation. In 18 heptapeptides, in which L10 or G9 was replaced, three peptides caused salivation but none had significantly increased secretory activities. In 18 heptapeptides in which Y8 was replaced, four caused salivation but only one (I) had significantly increased secretory activity. In 18 heptapeptides in which F7 was replaced, only Y caused salivation but with significantly reduced secretory activity. In contrast, in 18 heptapeptides in which K6 and N5 were replaced, most caused salivation and some of them had significantly increased secretory activities. CONCLUSIONS: It is concluded that the sequence FYGLM-NH2 conserved in the C-terminal region of physalaemin is optimal, that amides in position II and F7 are very important for salivation, but that K6 and N5 can be replaced by some other amino acids, resulting in increased secretory activities.

Amino Acids↗