NE inhibits cerebrovascular mast cell exocytosis induced by cholinergic and peptidergic agonists
| Autor: | P. Aubineau, Jacques Callebert, Jacques Seylaz, Jean-Marie Launay, A. M. Reynier-Rebuffel |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Male
Adrenergic Antagonists Serotonin medicine.medical_specialty Physiology In Vitro Techniques Biology Exocytosis Muscle Smooth Vascular Norepinephrine chemistry.chemical_compound Physiology (medical) Internal medicine medicine Animals Mast Cells Neurotransmitter Prazosin Cerebral Arteries Mast cell Kinetics Autonomic nervous system Endocrinology medicine.anatomical_structure Atenolol chemistry Cerebrovascular Circulation Timolol Cholinergic Carbachol Rabbits Acetylcholine medicine.drug |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 273:R845-R850 |
| ISSN: | 1522-1490 0363-6119 |
| DOI: | 10.1152/ajpregu.1997.273.3.r845 |
| Popis: | Autonomic and sensory nerves frequently contact mast cells contained in rabbit leptomeningeal arteries. We have previously shown that parasympathetic and peptidergic neurotransmitters can stimulate mast cell granule exocytosis and serotonin (5-HT) release. In the present study, we examined ex vivo the possible action of the main sympathetic neurotransmitter, norepinephrine (NE), on this exocytotic process. NE, which had no effect on mast cell 5-HT content per se, totally inhibited carbachol-induced 5-HT release and partially reduced neuropeptide-induced 5-HT release. Pretreatment with the alpha 1-adrenergic blocker did not affect the inhibitory effect of NE. Pretreatment with specific beta 1- or beta 2-adrenergic blockers antagonized this action, but the beta 2-blocker exerts a more specific dose-dependent antagonism. Together with our previous data, these results indicate that the equilibrium between autonomic and sensory nerves may determine the release of 5-HT from mast cells (parasympathetic and sensory nerves can trigger exocytosis while the sympathetics can inhibit it). Such a mechanism could be implicated in pathophysiological events in which autonomic dysfunction is likely to be involved, such as vascular headache or other phenomena involving inflammation. |
| Databáze: | OpenAIRE |
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