Inhibition of thromboxane and prostacyclin production in whole blood by adrenoceptor antagonists.
There is increasing evidence implicating thromboxane A2 (TxA2) in vascular disease. Adrenergic blocking agents have been used with success in the secondary prevention of myocardial infarction. The aim of this study was to determine whether adrenergic blocking agents had any effect on the production of TxA2 and prostacyclin (PGI2) from whole blood in vitro. Fresh whole blood without anticoagulant was placed in glass tubes containing either drug or vehicle, the latter acting as control, and allowed to clot at 37 degrees C for 30 minutes. The serum PGI2 metabolites (PGI2M) and TxB2 (the stable hydration product of TxA2) were determined by radioimmunoassay. Labetalol, pindolol and propranolol all inhibited both PGI2M and TxB2 production in a dose dependent manner, while atenolol had no effect. Labetalol was the most potent significantly inhibiting TxB2 production at a drug concentration compatible with that found in-vivo. This inhibitory effect on TxB2 production may be of benefit in the treatment of vascular disease.
Greer
I A
IA
Walker
J J
JJ
McLaren
M
M
Calder
A A
AA
Forbes
C D
CD
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D001262:Atenolol / Q000494:pharmacology; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D007741:Labetalol / Q000494:pharmacology; D010869:Pindolol / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D013928:Thromboxane A2 / Q000096:biosynthesis*; D013929:Thromboxane B2 / Q000096:biosynthesis
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D001262:Atenolol; D013929:Thromboxane B2; D013928:Thromboxane A2; D011433:Propranolol; D010869:Pindolol; D011464:Epoprostenol; D007741:Labetalol