Аннотация
Mast cells release histamine and other mediators of allergy in response
to stimulation of their IgE receptors. This release is generally
thought to be mediated by an elevation of cytosolic Ca2+. Recent
evidence suggests that there might be factors that modulate the coupling
between Ca2+ levels and mediator release. The present report identifies
adenosine as one such modulator. Adenosine and several of its metabolically
stable analogues were shown to enhance histamine release from rat
peritoneal mast cells in response to stimuli such as concanavalin
A. Metabolizing endogenous adenosine with adenosine deaminase dampened
the response to stimuli, whereas trapping endogenous adenosine inside
mast cells with nucleoside-transport inhibitors markedly enhanced
stimulated histamine release. The metabolically stable adenosine
analogue 5'-(N-ethylcarboxamido)adenosine (NECA) did not affect the
initial steps in the sequence from IgE-receptor activation to mediator
release, which are generation of inositol trisphosphate and increase
of cytosolic Ca2+. However, NECA did enhance the release induced
in ATP-permeabilized cells by exogenous Ca2+, but it had no effect
on the release induced by phorbol esters. These data suggest that
adenosine sensitizes mediator release by a mechanism regulating stimulus-secretion
coupling at a step distal to receptor activation and second-messenger
generation.
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