Norepinephrine Infusion

To study the possible role of catecholamines in platelet activation, platelet aggregation stimulated by AI?P, 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/mI (± SD), and plasma renin activity from 1.0 ± 0.5 to 4.2 ± 1.8 ng Al/ 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 blockade, platelet aggregation stimulated by ADP, l-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 ,tg/min) significantly reduced platelet aggregation with low-dose collagen (0.25-0.75 ,ug/ml), 1epinephrine (0.2-1.0 ,uM) and ADP (0.5-1.5 ,uM). These data do not support a role of endogenous catecholamines in initiating platelet activation and TXB2 formation.