Sub-aggregatory doses of catecholamines prevent prostacyclin-induced inhibition of platelet aggregation.
To assess the effect of subaggregatory concentrations of catecholamines on the antiaggregatory effect of prostacyclin (PGI2), platelets from normal human volunteers were exposed sequentially in vitro to epinephrine (less than or equal to 50 nM)- or norepinephrine (less than or equal to 1 microM) followed by PGI2 and adenosine diphosphate (ADP). Platelets thus pretreated did not manifest the normal inhibitory response to PGI2, aggregating to a similar extent as platelets exposed to ADP alone. This effect was unaffected by aspirin but was abolished by exposure to phentolamine. Catecholamine pretreatment similarly blocked the PGI2-induced increase in intracellular cyclic AMP, an effect which was also reversed by phentolamine. These data suggest that platelets exposed in vivo to elevated catecholamine concentrations, such as are seen clinically during myocardial infarction, might be similarly unresponsive to endogenous PGI2.
Buttrick
P M
PM
Forscher
C A
CA
Sussman
I I
II
Mueller
H S
HS
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000328:Adult; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000378:metabolism; D002395:Catecholamines / Q000494:pharmacology*; D000242:Cyclic AMP / Q000097:blood; D004837:Epinephrine / Q000494:pharmacology; D011464:Epoprostenol / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D010646:Phentolamine / Q000494:pharmacology; D010974:Platelet Aggregation / Q000187:drug effects*
D002395:Catecholamines; D000244:Adenosine Diphosphate; D011464:Epoprostenol; D000242:Cyclic AMP; D001241:Aspirin; D004837:Epinephrine; D010646:Phentolamine