Chong K P, Burch R M, Black M, Maloney E, Jollow D J, Halushka P V
Prostaglandins. 1983 Sep;26(3):397-408. doi: 10.1016/0090-6980(83)90175-2.
This study was designed to determine if vasopressin stimulates the formation of thromboxane B2 in freshly isolated hamster hepatocytes and if so, whether this thromboxane synthesis plays a role in the vasopressin-induced efflux of 45Ca++ from these cells. Thromboxane synthesis was found to be linear for 15 minutes, to be stimulated by arachidonic acid, and to be inhibited by indomethacin and by 7-(1-imidazolyl) heptanoic acid (7IHA), a selective inhibitor of thromboxane synthetase. Vasopressin stimulation of thromboxane synthesis was dose-related. Pretreatment with 7IHA and meclofenamate significantly increased basal 45Ca++ uptake by the cells. Neither 7IHA nor meclofenamate inhibited the ability of vasopressin to reduce the 45Ca++ content of the isolated hepatocytes. These results indicate that vasopressin stimulates thromboxane synthesis in hepatocytes but suggest that thromboxane does not play a role in the vasopressin-induced reduction in 45Ca++ content in this cell type.
本研究旨在确定血管加压素是否刺激新鲜分离的仓鼠肝细胞中血栓素B2的形成，若有刺激作用，该血栓素合成是否在血管加压素诱导的这些细胞中45Ca++流出中发挥作用。发现血栓素合成在15分钟内呈线性，受花生四烯酸刺激，并受吲哚美辛和血栓素合成酶的选择性抑制剂7-(1-咪唑基)庚酸（7IHA）抑制。血管加压素对血栓素合成的刺激呈剂量相关。用7IHA和甲氯芬那酸预处理显著增加了细胞对基础45Ca++的摄取。7IHA和甲氯芬那酸均未抑制血管加压素降低分离肝细胞中45Ca++含量的能力。这些结果表明血管加压素刺激肝细胞中的血栓素合成，但提示血栓素在这种细胞类型中血管加压素诱导的45Ca++含量降低中不发挥作用。
