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Effect of propranolol on platelet function
BB Weksler, M Gillick and J Pink
Excessive reactivity of blood platelets may contribute to atherosclerotic
vascular disease. Hence drugs which alter platelet function may be
protective. Prompted by findings that propranolol therapy normalized
hyperactive platelet aggregation in patients with coronary artery disease,
we studied propranolol in vitro to assess its action on platelets. At
concentrations similar to those achieved in vivo (0.1-1 muM), propranolol
raised the thresholds for aggregation of some normal paltelets by adenosine
diphosphate (ADP). At higher concentrations (10-50 muM), propranolol
abolished the second wave of platelet aggregation induced by ADP and
epinephrine, and inhibited aggregation induced by collagen, thrombin, and
the ionophore A23187. Propanolol blocked the release of 14C-serotonin from
platelets, inhibited platelet adhesion to collagen, and interfered with
clot retraction. Propranolol blocked ionophore-induced uptake of 45Ca by
platelets. Inhibition appeared unrelated to beta-adrenergic blockage, as
d(+) propranolol (which lacks beta-blocking activity) was equipotent with
1(-) propranolol. Moreover, practolol, a beta-blockading drug which is
nonlipophilic, did not inhibit platelet function. These studies suggested
that propranolol, like local anesthetics, decreased platelet responsiveness
by a direct action on the platelet membrane, possibly by interfering with
calcium availability. Modulation of platelet function by propranolol may
occur at concentrations achieved at usual clinical doses of the drug.
Volume 49,
Issue 2,
pp. 185-196,
02/01/1977
Copyright © 1977 by The American Society of Hematology
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