Nosál R, Jancinová V, Petríková M
Gen Physiol Biophys. 1983 Oct;2(5):353-62.
The inhibition of aggregation of rat platelets treated with betaadrenoceptor blocking drugs alprenolol, exaprolol, metipranolol, practolol and propranolol, and stimulated with adenosinediphosphate was shown to be dose-dependent. Atenolol in all concentrations potentiated the aggregation. The stimulated aggregation was potentiated by low and decreased by high concentrations of doberol. Cyclic adenosinemonophosphate was decreased in platelets treated with all the betaadrenoceptor blocking drugs used. On the other hand, a dose-dependent increase in the cyclic guanosinemonophosphate content was evident in betaadrenoceptor blocker-treated platelets. The interaction of betaadrenoceptor blocking drugs with the aggregation of blood platelets seems not to be mediated through cyclic nucleotides.
已表明,用β-肾上腺素受体阻断药阿普洛尔、依沙洛尔、美替洛尔、普拉洛尔和普萘洛尔处理并用二磷酸腺苷刺激的大鼠血小板聚集受到抑制,且呈剂量依赖性。所有浓度的阿替洛尔均增强聚集作用。低浓度的多贝洛尔增强刺激后的聚集,高浓度则降低聚集。在所使用的所有β-肾上腺素受体阻断药处理的血小板中,环磷酸腺苷均减少。另一方面,在β-肾上腺素受体阻断药处理的血小板中,环磷酸鸟苷含量呈剂量依赖性增加。β-肾上腺素受体阻断药与血小板聚集之间的相互作用似乎不是通过环核苷酸介导的。