Chloride efflux in cyclic AMP-induced configurational change of bovine pulmonary artery endothelial cells.
Chloride efflux in cyclic AMP-induced configurational change of bovine pulmonary artery endothelial cells.
复制标题
环AMP诱导的牛肺动脉内皮细胞构型变化中的氯离子流出。
DOI：
10.1161/01.res.66.4.957
复制
发表时间：
1990
影响因子：
20.1
通讯作者：
Fanburg,BL
中科院分区：
文献类型：
--
作者：
Ueda,S;Lee,SL;Fanburg,BL
通过异丙肾上腺素和3-异丁基-1-甲基黄嘌呤等药物升高细胞环AMP，使单层牛肺动脉内皮细胞快速可逆地形成树突状。将细胞暴露于多种其他血管活性剂、钙离子载体、佛波酯或环GMP中，则不会出现这种效果。2.5 mM n -苯氰苯甲酸或145 mM葡萄糖酸钠（Cl-通道抑制剂）完全抑制环amp诱导的构型变化，2.5 mM 4-乙酰氨基-4'-异硫氰酸二苯乙烯-2,2'-二磺酸（SITS）部分抑制环amp诱导的构型变化，但Ca2+或Na+离子剥夺、1 mM布美他尼（Cl-共转运抑制剂）、1 mM阿米洛利（Na+/H+交换抑制剂）、0.1 mM维拉帕米（Ca2+通道抑制剂）或5 mM BaCl2 （K+通道抑制剂）对环amp诱导的构型变化不受影响。通过改变细胞pH值或百日咳毒素。三氟哌嗪（钙调素抑制剂，50微米）、1毫米EGTA加100微米3,4,5-三甲氧基苯甲酸8-（二乙胺）辛酯（TMB-8，细胞内Ca2+拮抗剂）和5微米细胞松弛素B也能产生细胞收缩，但这些变化不被氯通道抑制所阻断。在0.1 mM瓦阿因加0.1 mM布美他胺的情况下，异丙肾上腺素加异丁基甲基黄嘌呤可降低36Cl-的摄取，增强其外排。n -苯氰苯甲酸抑制刺激外排。我们得出结论，环状AMP诱导内皮细胞的构型变化，这与细胞的Cl-外排有关；细胞效应可能在血管功能中起作用。
Elevation of cellular cyclic AMP by agents such as isoproterenol plus 3-isobutyl-1-methylxanthine produced rapid and reversible dendritic formation of bovine pulmonary artery endothelial cells in the monolayer. The effect did not occur with exposure of the cells to a variety of other vasoactive agents, calcium ionophore, phorbol ester, or cyclic GMP. The cyclic AMP-induced configurational change was completely inhibited by 2.5 mM N-phenylanthranilic acid or 145 mM sodium gluconate (Cl- channel inhibitors) and was partially inhibited by 2.5 mM 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS), but it was not affected by deprivation of Ca2+ or Na+ ion, 1 mM bumetanide (Cl- cotransport inhibitor), 1 mM amiloride (Na+/H+ exchange inhibitor), 0.1 mM verapamil (Ca2+ channel inhibitor), or 5 mM BaCl2 (K+ channel inhibitor), by change in cellular pH, or by pertussis toxin. Trifluoperazine (calmodulin inhibitor, 50 microM), 1 mM EGTA plus 100 microM 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8, intracellular Ca2+ antagonist), and 5 microM cytochalasin B also produced cellular retraction, but these changes were not blocked by chloride channel inhibition. In the presence of 0.1 mM ouabain plus 0.1 mM bumetanide, 36Cl- uptake was decreased by isoproterenol plus isobutylmethylxanthine while its efflux was enhanced. N-Phenylanthranilic acid inhibited the stimulated efflux. We conclude that cyclic AMP induces a configurational change of endothelial cells that is related to Cl- efflux from the cells; the cellular effects may play a role in vascular function.