Circulation, Vol 66, 44-48, Copyright © 1982 by American Heart Association
W Siess, R Lorenz, P Roth and PC Weber
To study the possible role of catecholamines in platelet activation,
platelet aggregation stimulated by ADP, collagen, arachidonic acid and
L-epinephrine, thromboxane B2 (TXB2) formation and plasma levels of
catecholamines and renin were studied in healthy men both before and after
6 days of propranolol treatment (40 mg three times daily) under control
conditions and during sympathoadrenergic stimulation by physical exercise
(200 W) or smoking. Exercise markedly increased plasma norepinephrine from
128 +/- 28 to 998 +/- 418 pg/ml (+/- SD), and plasma renin activity from
1.0 +/- 0.5 to 4.2 +/- 1.8 ng AI/ml . hour. Smoking predominantly increased
plasma epinephrine, from 47 +/- 25 to 154 +/- 76 pg/ml. Propranolol did not
consistently influence these variables, but blunted the circulatory
response to exercise and smoking. Despite the marked increases of plasma
catecholamines after both stimuli with and without beta blockade, platelet
aggregation stimulated by ADP, 1-epinephrine, collagen and arachidonic acid
and associated TXB2 formation were not enhanced. Moreover, as already
suggested by a trend toward reduced aggregability in these settings, plasma
norepinephrine levels in the same range (745 +/- 368 pg/ml) due to infusion
(5 micrograms/min) significantly reduced platelet aggregation with low-dose
collagen (0.25-0.75 micrograms/ml), I- epinephrine (0.2-1.0 microM) and ADP
(0.5-1.5 microM). These data do not support a role of endogenous
catecholamines in initiating platelet activation and TXB2 formation.
ARTICLES
Plasma catecholamines, platelet aggregation and associated thromboxane formation after physical exercise, smoking or norepinephrine infusion
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