Dalen T, Vestereng M, Wadsworth R, Kane K
Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, Scotland, UK.
Eur J Pharmacol. 1994 Aug 3;270(4):313-9. doi: 10.1016/0926-6917(94)90007-8.
The thromboxane mimetic U46619 (11 alpha,9 alpha-epoxymethano PGH2) increased 45Ca2+ uptake in sheep coronary artery rings. A larger increase occurred in endothelium-denuded than in endothelium-inact rings (increase in 45Ca2+ uptake: endothelium intact = 9.6 +/- 3.8, endothelium-denuded = 33.2 +/- 8.1 nmol g-1), in agreement with the increase in U46619 contraction produced by endothelium denudation. Hypoxia (PO2 = 4 mm Hg) inhibited both the U46619 contraction (at the U46619 EC50, contraction under oxygenated conditions = 158 +/- 35, under hypoxic conditions = 105 +/- 40 g cm-2) and the U46619-stimulated 45Ca2+ uptake. It is concluded that inhibition, by hypoxia, of the U46619 contractile effect on sheep coronary artery rings may be in part due to inhibition of U46619-stimulated 45Ca2+ uptake.
血栓素类似物U46619（11α,9α-环氧甲撑前列环素H2）可增加绵羊冠状动脉环对45Ca2+的摄取。与内皮完整的环相比，内皮剥脱的环中45Ca2+摄取增加更为显著（45Ca2+摄取增加量：内皮完整 = 9.6 ± 3.8，内皮剥脱 = 33.2 ± 8.1 nmol g-1），这与内皮剥脱导致U46619收缩增强一致。缺氧（PO2 = 4 mmHg）既抑制U46619收缩（在U46619半数有效浓度时，氧合条件下收缩 = 158 ± 35，缺氧条件下 = 105 ± 40 g cm-2），也抑制U46619刺激的45Ca2+摄取。结论是，缺氧对绵羊冠状动脉环U46619收缩效应的抑制可能部分归因于对U46619刺激的45Ca2+摄取的抑制。
