ADENOSINE-TRIPHOSPHATE STIMULATES INOSITOL PHOSPHOLIPID-METABOLISM AND PROSTACYCLIN FORMATION IN ADRENAL-MEDULLARY ENDOTHELIAL-CELLS BY MEANS OF P2-PURINERGIC RECEPTORS
ADENOSINE-TRIPHOSPHATE STIMULATES INOSITOL PHOSPHOLIPID-METABOLISM AND PROSTACYCLIN FORMATION IN ADRENAL-MEDULLARY ENDOTHELIAL-CELLS BY MEANS OF P2-PURINERGIC RECEPTORS
复制标题
DOI：
10.1073/pnas.84.16.5630
复制
发表时间：
1987-08-01
影响因子：
11.1
通讯作者：
POLLARD, HB
中科院分区：
文献类型：
--
作者：
FORSBERG, EJ;FEUERSTEIN, G;POLLARD, HB
在肾上腺髓质中，嗜铬细胞分泌高浓度的儿茶酚胺、ATP、肽和其他必须穿过内皮细胞屏障进入血流的因子。我们已经测量了几个这些嗜铬细胞分泌产物对培养的牛肾上腺髓质内皮细胞的影响，并发现只有ATP刺激前列环素的形成。ATP对前列环素形成的刺激与肌醇磷脂的代谢和推定的第二信使三磷酸肌醇的积累相一致。ATP刺激的前列环素形成和ATP刺激的肌醇磷脂代谢的时间过程，浓度依赖性和P2-嘌呤能受体特异性相似。因此，前列环素形成的增加可能是继发于三磷酸肌醇对细胞内Ca 2+的动员，导致磷脂酶A2的活化，花生四烯酸的释放，以及花生四烯酸向前列环素的转化。我们认为ATP的功能可能是通过与邻近的内皮细胞相互作用来调节肾上腺髓质和其他内分泌组织中的血流，ATP通常与分泌细胞中的细胞特异性激素共定位。
In the adrenal medulla, chromaffin cells secrete high concentrations of catecholamines, ATP, peptides and other factors that must pass through an endothelial cell barrier to enter the bloodstream. We have measured the effect of several of these chromaffin cell secretory products on cultured bovine adrenal medullary endothelial cells and have found that only ATP stimulates prostacyclin formation. The stimulation of prostacyclin formation by ATP coincides with the metabolism of inositol phospholipids and the accumulation of the putative second messenger inositol trisphosphate. The time course, concentration dependence, and P2-purinergic receptor specificity were similar for ATP-stimulated prostacyclin formation and ATP-stimulated inositol phospholipid metabolism. Thus, the increase in prostacyclin formation may be secondary to mobilization of intracellular Ca2+ by inositol trisphosphate, leading to activation of phospholipase A2, liberation of arachidonic acid, and the conversion of arachidonic acid to prostacyclin. We propose that the function of ATP, which is often colocalized with cell-specific hormones in secretory cells, may be to regulate blood flow in the adrenal medulla and other endocrine tissues by interacting with adjacent endothelial cells.