Selheim F, Frøyset A K, Strand I, Vassbotn F S, Holmsen H
Department of Biochemistry and Molecular Biology, University of Bergen, Norway.
FEBS Lett. 2000 Nov 17;485(1):62-6. doi: 10.1016/s0014-5793(00)02188-8.
Adrenaline significantly potentiated late thrombin- and SFRLLN-induced PtdIns(3,4)P(2) production. Furthermore, the potentiating effect of adrenaline on thrombin-induced PtdIns(3, 4)P(2) production was independent on secreted ADP, whereas, the effect of adrenaline on SFRLLN-induced PtdIns(3,4)P(2) production was completely dependent of secreted ADP. However, the ADP-dependent accumulation of PtdIns(3,4)P(2) was not required for irreversible platelet aggregation induced by SFRLLN in the presence of adrenaline. It is concluded that adrenaline can replace secreted ADP to potentiate PtdIns(3,4)P(2) production in thrombin-stimulated but not in SFRLLN-stimulated platelets, thus demonstrating a qualitative difference between platelet stimulation by thrombin and the thrombin receptor activating peptide SFRLLN.
肾上腺素显著增强了晚期凝血酶和SFRLLN诱导的磷脂酰肌醇(3,4)二磷酸(PtdIns(3,4)P(2))的生成。此外,肾上腺素对凝血酶诱导的PtdIns(3,4)P(2)生成的增强作用不依赖于分泌的ADP,而肾上腺素对SFRLLN诱导的PtdIns(3,4)P(2)生成的作用则完全依赖于分泌的ADP。然而,在肾上腺素存在的情况下,SFRLLN诱导的不可逆血小板聚集并不需要依赖ADP的PtdIns(3,4)P(2)积累。得出的结论是,肾上腺素可以替代分泌的ADP来增强凝血酶刺激而非SFRLLN刺激的血小板中PtdIns(3,4)P(2)的生成,从而证明了凝血酶和凝血酶受体激活肽SFRLLN刺激血小板之间的质性差异。