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Epinephrine induces platelet fibrinogen receptor expression, fibrinogen
binding, and aggregation in whole blood in the absence of other excitatory
agonists
SJ Shattil, A Budzynski and MC Scrutton
Department of Medicine, University of Pennsylvania School of Medicine,
Philadelphia 19104.
The exposure of fibrinogen receptors is an early event in agonist- induced
platelet activation. Previous measurements of fibrinogen binding or
aggregation in platelet-rich plasma or washed platelets have failed to
define whether the initial response to epinephrine results solely from a
direct effect of this agonist. To address this problem, we have measured
fibrinogen receptor exposure on platelets in whole blood by using flow
cytometry and a fluorescein isothiocyanate-labeled monoclonal antibody
specific for the activated fibrinogen receptor (FITC-PAC1). We also
measured platelet-bound fibrinogen with an antifibrinogen monoclonal
antibody (FITC-9F9) as well as platelet aggregation in whole blood. In
blood anticoagulated with citrate and in the presence of a cyclooxygenase
inhibitor, epinephrine (0.1 to 100 mumol/L) caused significant FITC-PAC1
binding (P less than .001) that was maximal at 10 mumol/L epinephrine. The
maximal epinephrine response was one third of that observed with 10 mumol/L
adenosine diphosphate (ADP) and was eliminated by yohimbine, an alpha
2-adrenergic antagonist. Incubation of the blood with apyrase or
phosphoenolpyruvate plus pyruvate kinase to remove extracellular ADP
resulted in a 40% to 50% reduction in the epinephrine response. Despite
this, FITC-PAC1 binding was still significant at epinephrine greater than
or equal to 1 mumol/L (P less than .05). No reduction in
epinephrine-induced FITC- PAC1 binding was observed in the presence of ATP
alpha S, an ADP receptor antagonist; cinanserin, a serotonin antagonist; or
WEB-2086, a platelet activating factor antagonist. Furthermore, addition of
the thrombin inhibitors hirudin or leupeptin to citrated blood had no
effect on the extent of the epinephrine response. Blood anticoagulated with
hirudin also demonstrated an epinephrine response, even in the presence of
apyrase. Similar results were obtained when FITC-9F9 was used to detect
fibrinogen binding or when aggregation was assessed by a decrease in the
number of single platelets. We conclude that epinephrine itself can induce
fibrinogen receptor exposure, fibrinogen binding, and aggregation. This
primary response is independent of synergistic interaction of epinephrine
with traces of ADP, serotonin, platelet activating factor, or thrombin.
However, such synergistic interaction with ADP present in whole blood may
enhance the responses induced by epinephrine.
Volume 73,
Issue 1,
pp. 150-158,
01/01/1989
Copyright © 1989 by The American Society of Hematology
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