AJP - Regulatory, Integrative and Comparative Physiology, Vol 245, Issue 1 100-R109, Copyright © 1983 by American Physiological Society
Regulation of canine platelet function II. Catecholamines
K. M. Meyers, L. Y. Huston and R. M. Clemmons
The action of epinephrine (E) on canine platelet aggregation is described.
Although E did not induce a change in platelet shape or aggregation,
potentiation of aggregation induced by the following agents was observed at
physiological E concentrations (that is, less than 10 nM/1): arachidonic
acid; the dense granule agonists, ADP and serotonin (5-HT); and collagen.
Epinephrine-induced potentiation was in part independent of formation of
arachidonic acid metabolites, and E potentiated the aggregating action of
the bivalent cationophore A23187. Potentiation was inhibited by
alpha-adrenergic receptor antagonists phenoxybenzamine, phentolamine, and
ergotamine, and mimicked by alpha-adrenergic receptor agonists
norepinephrine, clonidine, and in some cases, phenylephrine. The
beta-adrenergic receptor agonists isoproterenol and dobutamine inhibited
ADP-induced aggregation, and this action was presented by pretreating the
platelets with propranolol and dichloroisoproterenol. An augmentation of
the aggregation response of platelets to arachidonic acid was observed in
blood samples withdrawn when circulating catecholamines were elevated. The
physiological implication of epinephrine acting as a gain controller that
alters the relationship between actuating signal and the platelet response
to an agonist is discussed.
