Akiba S, Sato T, Fujii T
Department of Biochemistry, Kyoto Pharmaceutical University, Japan.
Biochem Mol Biol Int. 1993 Sep;31(1):135-42.
A mechanism by which vasopressin enhances phospholipase A2 activation in rabbit platelets was investigated. Stimulation of the platelets with vasopressin enhanced arachidonic acid liberation, as well as aggregation and ATP secretion in the presence of submaximal concentration of A23187, although vasopressin alone had no effect. The vasopressin-enhanced liberation was inhibited by p-bromophenacyl bromide, a phospholipase A2 inhibitor, and by genistein, a tyrosine kinase inhibitor. Though epinephrine also caused a similar enhancement of the liberation, this effect of epinephrine was insensitive to genistein. Staurosporine, a protein kinase C inhibitor, completely suppressed phorbol 12-myristate 13-acetate-enhanced arachidonic acid liberation, but suppressed the vasopressin-induced enhancement only slightly. These results suggest that vasopressin-enhanced phospholipase A2 activation may be regulated by a genistein-sensitive mechanism, most likely by a protein tyrosine kinase-mediated pathway, but not by guanine nucleotide-binding protein- or protein kinase C-mediated pathway.
研究了血管加压素增强兔血小板中磷脂酶A2活性的机制。尽管血管加压素单独作用时无效果，但在亚最大浓度的A23187存在下，用血管加压素刺激血小板可增强花生四烯酸的释放以及聚集和ATP分泌。磷脂酶A2抑制剂对溴苯甲酰溴和酪氨酸激酶抑制剂染料木黄酮可抑制血管加压素增强的释放。虽然肾上腺素也能引起类似的释放增强，但肾上腺素的这种作用对染料木黄酮不敏感。蛋白激酶C抑制剂星形孢菌素可完全抑制佛波醇12-肉豆蔻酸酯13-乙酸酯增强的花生四烯酸释放，但对血管加压素诱导的增强作用仅略有抑制。这些结果表明，血管加压素增强的磷脂酶A2激活可能受染料木黄酮敏感机制的调节，最有可能是由蛋白酪氨酸激酶介导的途径，而不是由鸟嘌呤核苷酸结合蛋白或蛋白激酶C介导的途径。
