Chronic pain treatment: the influence of tricyclic antidepressants on serotonin release and uptake in mast cells.

The involvement of serotonin (5-HT) in chronic pain mechanisms is established. 5-HT inhibits central painful stimuli, but recent data suggests that 5-HT could also enhance pain stimulus from the periphery, where mast cells play an important role. We aimed in our study to clarify the influence of selected tricyclic antidepressants (TCAs) on mast cell function: secretion, uptake, and reuptake of 5-HT, that could interfere with 5-HT levels and in this way contribute to the generation of pain.

Histamine release, an undesired effect of thrombin inhibitors with basic character, is mediated through direct activation of G(i) proteins.

The common structural feature of LK direct thrombin inhibitors is a strong basic group attached to the azaphenylalanine scaffold, which is important for the appropriate interaction at the thrombin active site. Our previous results have shown that this basic group could be responsible for a reduction of tracheal air flow and a fall of mean arterial pressure in anaesthetized rats, an undesired effect of direct thrombin inhibitors which correlated with their ability to release histamine from mast cells. In the present study, we investigated the mechanism of LK direct thrombin inhibitors-induced histamine release from rat peritoneal mast cells.

Signaling pathway in nerve growth factor induced histamine release from rat mast cells.

Objective And Design: We investigated a signal transduction pathway involved in NGF induced histamine secretion from mast cells. We compared this mechanism with the exocytosis induced by basic secretagogue compound 48/80.

Materials And Methods: Isolated rat peritoneal mast cells were obtained from male Wistar rats.

Regulatory role of extracellular Na+ and Ca2+ ions in nerve growth factor induced histamine secretion from rat mast cells.

Objective And Design: This study was aimed to investigate effects of extracellular Na+ and Ca2+ ions on nerve growth factor (NGF) induced histamine release from mast cells.

Material: Isolated peritoneal mast cells were obtained from male Wistar rats.

Methods: Cells were suspended in solution with different concentration of Na+ and Ca2+ ions and stimulated with NGF.

The influence of Na+ ions on histamine secretion from mast cells induced by NGF or compound 48/80.

It has been demonstrated that the release of histamine from mast cells by cytokines is strongly dependent on extracellular Ca2+ and Na+ ions. The results of our current research indicate that the removal of extracellular Na+ enhances NGF induced histamine release, but reduces induction by compound 48/80, suggesting that different mechanisms are involved in the secretory process induced by these agents.

Changes in histamine and serotonin secretion from rat peritoneal mast cells caused by antidepressants.

Psychotropic agents modify the release of histamine and serotonin from rat peritoneal mast cells induced by compound 48/80. Some antidepressants, such as clomipramine and fluoxetine (10(-8) - 10(-5) mol/l), increase the percentage of released serotonin in the incubation medium but have no effect on histamine release. In contrast, amitriptyline (10(-4) mol/l) inhibits the secretion of histamine and permits that of serotonin.

The mechanism of histamine release induced by pilocarpine from different tissues: studies on rat peritoneal mast cells.

Pilocarpine releases histamine from mast cells of cat submandibular gland and rat liver. In the salivary gland, histamine is released into the saliva and venous outflow. Atropine blocks the salivation, but not histamine release from the submandibular gland into the blood.

Effect of ouabain, digoxin and digitoxigenin on potassium uptake and histamine release from rat peritoneal mast cells.

Rat peritoneal mast cells were used to study the effects of digitalis glycosides on potassium uptake and histamine release induced by compound 48/80, substance P and egg-albumin (immunological release). In the absence of calcium all glycosides inhibited potassium uptake. Ouabain and digoxin enhanced the histamine release while digitoxigenin either had no effect or was slightly inhibitory.

Activation of the Na+/K(+)-pump in rat peritoneal mast cells following histamine release: a possible role in cell recovery.

1. The activity of the Na+/K(+)-pump in rat peritoneal mast cells was measured at various time intervals after induction of cellular histamine release by compound 48/80 or by the antigen-antibody reaction. The Na+/K(+)-pump activity was assessed as the ouabain-sensitive potassium uptake of the cells using 86Rb+ as a tracer for potassium (K+(86Rb+)-uptake).

Characteristics of histamine and serotonin release from rat mast cells induced by thymic peptides.

Thymopoietin peptides release histamine and serotonin from rat mast cells. The release has the characteristics of other basic secretagogues in that it occurs rapidly, does not require extracellular Ca2+ ions, and is inhibited by benzalkonium chloride (BAC). These similarities indicate that chemically different basic compounds have common mechanisms for histamine and serotonin release from rat mast cells.

Changes in histamine secretion from mast cells caused by digitalis glycosides.

Cardiotonic glycosides modify histamine secretion from rat mast cells in the following way. (1) Preincubation (30 min) of mast cells with liposoluble glycosides (10(-4) mol/l) increases the spontaneous histamine secretion by about 5%. (2) Preincubation of mast cells with 10(-4) mol/l liposoluble glycosides (digitoxin, digoxin, digitoxigenine) decreases histamine release induced by compound 48/80 in the presence of calcium, whereas the water soluble glycoside, strophanthin G, has no effect on the secretion.