Influence of some beta blockers (pindolol, atenolol, timolol and metoprolol) on aggregation and arachidonic acid metabolism in human platelets

Prostaglandins, leukotrienes, and medicine Pub Date : 1987-09-01 DOI:10.1016/0262-1746(87)90099-0

K.C. Srivastava

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引用次数: 18

Abstract

The effects of four beta-adrenoceptor blocking agents on platelet aggregation, formation of thromboxane from exogenous arachidonic acid (AA) in platelets, on AA incorporation in platelet phospholipids, and on platelet phospholipase activity were studied. Of the four drugs pindolol inhibited thromboxane formation in a dose-related (0.25–1.0 mM) manner apparently by exerting its influence at the cyclooxygenase (CO) level. This drug also inhibited aggregation induced by AA, collagen, epinephrine and ADP. Atenolol and metoprolol though not showing inhibition of AA-induced aggregation did inhibit collagen- and ADP-induced aggregation; metoprolol reversed ADP-induced aggregation, and abolished second phase of epinephrine-induced aggregation. Timolol did not inhibit aggregation induced by all the aggregating agents. Atenolol inhibited (by ca. 1096) TxB₂ formation in platelets from exagenous as well as endogenous AA at rather high concentrations (1.0 mM). Metoprolol and Tmolol did not do so. The observations reported here can be best explained by taking into account the membrane stabilizing effects and lipophilic properties of the drugs.

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一些受体阻滞剂(品多洛尔、阿替洛尔、替马洛尔和美托洛尔)对人血小板聚集和花生四烯酸代谢的影响

研究了四种β -肾上腺素受体阻滞剂对血小板聚集、外源性花生四烯酸(AA)在血小板中形成血栓烷、AA在血小板磷脂中的掺入以及血小板磷脂酶活性的影响。在四种药物中，品多洛尔明显通过对环氧化酶(CO)水平的影响，以剂量相关(0.25-1.0 mM)的方式抑制血栓素的形成。对AA、胶原、肾上腺素、ADP诱导的聚集也有抑制作用。阿替洛尔和美托洛尔虽然没有抑制aa诱导的聚集，但对胶原和adp诱导的聚集有抑制作用;美托洛尔逆转adp诱导的聚集，并消除肾上腺素诱导的第二阶段聚集。替莫洛尔对所有聚集剂诱导的聚集均无抑制作用。阿替洛尔在相当高的浓度(1.0 mM)下抑制(约1096)外源性和内源性AA在血小板中形成TxB2。美托洛尔和特摩洛尔则没有。考虑到药物的膜稳定作用和亲脂性，这里报告的观察结果可以得到最好的解释。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Prostaglandins, leukotrienes, and medicine

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