Anti-platelet activity of beta-adrenergic antagonists: inhibition of thromboxane synthesis and platelet aggregation in patients receiving long-term propranolol treatment.
Treatment of hypertensive patients with dl-propranolol (640 mg/day) significantly inhibited thromboxane synthesis by their platelets and platelet aggregation induced by thrombin or arachidonic acid. The effects were dose-related and were also caused by the stereoisomer, d-propranolol (640 mg/day), which has very little beta-blocking activity. These findings suggest that the cardioprotective effects of propranolol may be due partly to this anti-platelet activity, to a reduction in thromboxane-induced coronary-artery vasoconstriction, or to both. d-Propranolol treatment may be particularly useful, since this isomer provides similar benefits without causing pronounced beta-adrenergic blockade.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000328:Adult; D002986:Clinical Trials as Topic; D003864:Depression, Chemical; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D011433:Propranolol / Q000008:administration & dosage / Q000627:therapeutic use; D011897:Random Allocation; D013237:Stereoisomerism; D013931:Thromboxanes / Q000096:biosynthesis*; D013997:Time Factors
D000319:Adrenergic beta-Antagonists; D013931:Thromboxanes; D011433:Propranolol