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Regulation of mast cell histamine release by neurotensin

Life Sciences, ISSN: 0024-3205, Vol: 31, Issue: 6, Page: 509-516
1982
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Neurotensin (NT), a neuropeptide found both centrally and peripherally, stimulated release of histamine from rat peritoneal mast cells in a dose-dependent manner. Release was evident by 10 nM and reached a plateau of 15–20% total cellular histamine by 10 −7 –10 −6 M NT. Optimal conditions for stimulation occurred at pH 6.5–7.5, 37°C and at calcium concentrations of ≤1 mM. Release was complete within 2 minutes of peptide addition. Studies of histamine release by NT analogues indicated that the C-terminus is the biologically active portion of the molecule in this system, as is true of all other systems responsive to NT (1). D-Trp 11 -NT, which acts as a NT antagonist in several peripheral NT-sensitive tissues (2,3), also inhibited NT action on mast cells. Manipulations involving Ca 2+ availability suggest that the mechanism of NT stimulation may involve use of intracellular Ca 2+ to a greater extent than extracellular Ca 2+. Lowering the extracellular Ca 2+ concentration or blocking influx of extracellular Ca 2+ with lanthanum (La 3+ ), had little effect on NT-induced release, whereas Ca 2+ depletion by treatment with ethylenediaminetetracetic acid (EDTA) or blockade of intracellular Ca 2+ mobilization by N,N-(diethylamino)octyl 3,4,5-trimethoxybenzoate (TMB-8), inhibited the response to NT. Increasing cellular levels of adenosine 3′, 5′-cyclic monophosphate (cAMP), by treatment with 8-bromo-cAMP or stimulation with prostaglandin E 2 (PGE 2 ) in the presence of isobutylmethylxanthine (IBMX), served to reduce histamine release by NT, indicating that cAMP may play a role in NT stimulation.

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