Anti-platelet activity of beta-adrenergic antagonists: inhibition of thromboxane synthesis and platelet aggregation in patients receiving long-term propranolol treatment. Lancet 1981 Dec 19-26;2(8260-61):1382-4
Date
12/19/1981Pubmed ID
6118758DOI
10.1016/s0140-6736(81)92800-2Scopus ID
2-s2.0-0019864989 (requires institutional sign-in at Scopus site) 105 CitationsAbstract
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.
Author List
Campbell WB, Johnson AR, Callahan KS, Graham RMAuthor
William B. Campbell PhD Professor in the Pharmacology and Toxicology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Adrenergic beta-AntagonistsAdult
Clinical Trials as Topic
Depression, Chemical
Dose-Response Relationship, Drug
Female
Humans
Hypertension
Male
Middle Aged
Platelet Aggregation
Propranolol
Random Allocation
Stereoisomerism
Thromboxanes
Time Factors
