Fluid Secretion In Salivary Glands Research Articles

Salivary gland fluid secretion during aging.

Salivary gland function is generally well-preserved in healthy older persons. Similar results are observed in the laboratory rat. Older people are, however, more likely to experience salivary disorders due to disease or its treatment. For many patients with remaining salivary gland parenchymal tissue, improved function may result from pharmacological therapy.

Regulation of calcium handling by rat parotid acinar cells.

Salivary gland fluid secretion following neurotransmitter stimulation is Ca2+-dependent. We have studied the control of cellular Ca2+ following secretory stimuli in rat parotid gland acinar cells. After muscarinic-cholinergic receptor activation, cytosolic Ca2+ is elevated 4-5 fold, due to both intracellular Ca2+ pool mobilization and extracellular Ca2+ entry. Fluid movement ensues due to the Ca2+-activated enhancement of membrane permeability to K+ and Cl-. Basal cytosolic Ca2+ levels are tightly controlled at approximately 150-200 nM through the action of high affinity and high capacity ATP-dependent Ca2+ transporters in the basolateral and endoplasmic reticulum membranes. Activity of these Ca2+ transporters can be modulated to facilitate rapid responsiveness and a sustained fluid secretory response necessary for alimentary function.

Potentiation of salivary fluid secretion in ixodid ticks: a new receptor system for gamma-aminobutyric acid.

gamma-Aminobutyric acid (GABA), having minimal intrinsic activity, potentiates dopamine-induced fluid secretion in salivary glands of female ixodid ticks. Because the effect of GABA was similar to that of spiperone, we tested whether these two drugs act at a common recognition site. Potentiation was not augmented when salivary glands were exposed to supramaximal concentrations of spiperone (1 microM) plus GABA (100 microM). (+/-)-Sulpiride (100 microM), a spiperone antagonist in this system, also blocked GABA-induced potentiation. Picrotoxin (100 microM) and (-)-bicuculline (100 microM), two GABA antagonists, blocked GABA-induced and spiperone-induced potentiation. Inhibition of GABA by picrotoxin and (-)-bicuculline was noncompetitive. Muscimol (an agonist at GABAA receptors) also potentiated dopamine-induced secretion. Baclofen (an agonist at GABAB receptors) did not elicit potentiation. We suggest that GABA may function as a neuromodulator for dopamine-induced fluid secretion in tick salivary glands.

Evidence for multiple receptors mediating fluid secretion in salivary glands of ticks

Using isolated salivary glands of the ixodid tick Amblyomma hebraeum Koch, we tested the effectiveness of butaclamol and sulpiride in blocking fluid secretion stimulated by a number of agonists. (+)-Butaclamol was a potent inhibitor of dopamine, N-methyldopamine and noradrenaline (K i ≅ 30–60 nM), but was less effective on ergometrine (K i ≅ 310 nM). Tranylcypromine-stimulated fluid secretion in the absence and presence of (+)-butaclamol and (±)-sulpiride suggested that tranylcypromine's action is mediated through two receptors. (±)-Sulpiride, though a rather weak antagonist of ergometrine (K i ≅ 6150 nM), was ineffectual as a dopamine blocker, indicating distinct receptor sites on this epithelium for dopamine and ergometrine. Both (+)-butaclamol and sulpiride reversed the autoinhibition associated with supramaximal levels of dopamine. Sulpiride also abolished spiperone's potentiation of dopamine. Butaclamol, on the other hand, had no such effect on spiperone's potentiation of dopamine. Finally, although the CNS of ticks contains both dopamine and noradrenaline in quantity (≅650 and ≅370 ng · g −1 respectively), the salivary glands contain far more dopamine than noradrenaline (≅85 and ≅6 ng · g −1 respectively). The data support the hypothesis that dopamine is a natural transmitter substance in the tick salivary gland, and that there are distinct receptor sites in the epithelium mediating the actions of catecholamines, ergot alkaloids and butyrophenones. The physiological significance of the ergot alkaloid and butyrophenone sites is not clear.