Antiplatelet activity of carvedilol in comparison to propranolol

The non-selective vasodilating g -blocker carvedilol was found to inhibit platelet aggregation as well as thromboxane B 2 formation more effectively than propranolol. The antiaggregatory activity of carvedilol decreased, depending on the stimulus used, in the following rank order of potency (in pare...

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Bibliographic Details
Published in:Platelets (Edinburgh) 2002-12, Vol.13 (8), p.479-485
Main Authors: Petríková, M., Jancinová, V., Nosál, R., Májeková, M., Danihelová, E.
Format: Article
Language:English
Subjects:
Adenosine Diphosphate - pharmacology
Calcimycin - pharmacology
Carbazoles - pharmacology
Dose-Response Relationship, Drug
In Vitro Techniques
Platelet Aggregation - drug effects
Platelet Aggregation - physiology
Platelet Aggregation Inhibitors - pharmacology
Propanolamines - pharmacology
Propranolol - pharmacology
Reference Values
Tetradecanoylphorbol Acetate - pharmacology
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Summary:The non-selective vasodilating g -blocker carvedilol was found to inhibit platelet aggregation as well as thromboxane B 2 formation more effectively than propranolol. The antiaggregatory activity of carvedilol decreased, depending on the stimulus used, in the following rank order of potency (in parentheses the respective mean inhibitory concentrations of carvedilol and propranolol are given in w mol/l): PMA (19 and 34) > thrombin (55 and 77) > Ca 2+ -ionophore A23187 (58 and 81) > epinephrine (86 and 118). However, aggregation of platelets activated with ADP was not affected by carvedilol in concentrations up to 100 w mol/l. In platelets stimulated with thrombin, carvedilol (10 w mol/l) reduced thromboxane B 2 formation by 64%, whereas propranolol was ineffective at this concentration. Moreover, A23187-induced formation of thromboxane B 2 , not affected by propranolol, was completely blocked by 100 w mol/l carvedilol. In comparison to propranolol, the molecule of carvedilol is more lipophilic and possesses lower dipole moment and higher molar refractivity, thus penetrating into platelet membranes readily and in large quantities. The antiplatelet effect was assumed to result from interactions of carvedilol with membrane macromolecules (phospholipids, ion channels, enzymes, etc.) rather than from blockade of f - and g -adrenergic receptors.
ISSN:0953-7104
1369-1635
DOI:10.1080/0953710021000057848