Bacic F, Uematsu S, McCarron R M, Spatz M
Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Prostaglandins Leukot Essent Fatty Acids. 1992 Jul;46(3):231-4. doi: 10.1016/0952-3278(92)90076-u.
Production of prostaglandin D2 (PGD2) was investigated in cultured endothelial cells derived from capillaries and microvessels (small and large) of human brain using radioimmunoassays. Peptides, catecholamines, thrombin, protein kinase C-activating phorbol ester and calcium ionophore greatly stimulated the secretion of endothelial PGD2. Secretion of PGD2 induced by vasoconstricting peptides, angiotensin II and arginine-vasopressin, was almost completely abolished by their respective specific receptor antagonists [Sar1, Ala8]-Ang II and [1-6(beta-mercapto-beta,beta-cyclopentamethylene propionic acid) 2-O-methyltyrosine]. Thus, the augmented production of PGD2 by angiotensin II and arginine-vasopressin is a receptor-mediated event. It also indicates that the EC have specific angiotensin II and arginine-vasopressin (V1) receptors. This study represents the first demonstration of vasoactive agents modulating PGD2 production in capillary and microvascular endothelium of human brain.
采用放射免疫分析法，对源自人脑毛细血管和微血管（大小血管）的培养内皮细胞中前列腺素D2（PGD2）的生成情况进行了研究。肽类、儿茶酚胺、凝血酶、激活蛋白激酶C的佛波酯以及钙离子载体均可极大地刺激内皮细胞分泌PGD2。血管收缩肽、血管紧张素II和精氨酸加压素所诱导的PGD2分泌，几乎可被其各自的特异性受体拮抗剂[Sar1，Ala8]-血管紧张素II和[1-6（β-巯基-β，β-环戊亚甲基丙酸）2-O-甲基酪氨酸]完全消除。因此，血管紧张素II和精氨酸加压素所致的PGD2生成增加是一个受体介导的事件。这也表明内皮细胞具有特异性的血管紧张素II和精氨酸加压素（V1）受体。本研究首次证明了血管活性药物可调节人脑毛细血管和微血管内皮细胞中PGD2的生成。
