Bacic F, Uematsu S, McCarron R M, Spatz M
Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.
Neurochem Res. 1992 Jul;17(7):699-702. doi: 10.1007/BF00968008.
Modulation of immunoreactive endothelin-1 (IR-ET-1) production by vasoactive substances was investigated in cultured endothelial cells (EC) derived from capillaries and microvessels of human brain. Peptides, catecholamines, thrombin, protein kinase C-activating phorbol ester, and calcium ionophore enhanced the secretion of IR-ET-1. The known vasoconstrictive peptides, angiotensin II (Ang II) and arginine-vasopressin (AVP) dose-dependently stimulated the endothelial secretion of IR-ET-1. The angiotensin and vasopressin-inducible production of IR-ET-1 was completely inhibited by their respective receptor antagonists [Sar1, Ala8]-angiotensin II and [1-6 (beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-O-methyl-tyrosine]. The results indicate that the peptide-stimulated secretion of IR-ET-1 is receptor-mediated in EC which have specific angiotensin II and arginine-vasopressin receptors. These findings represent the first demonstration of IR-ET-1 production by capillary and microvascular endothelium of human brain.
在源自人脑毛细血管和微血管的培养内皮细胞（EC）中，研究了血管活性物质对免疫反应性内皮素-1（IR-ET-1）产生的调节作用。肽类、儿茶酚胺、凝血酶、蛋白激酶C激活剂佛波酯和钙离子载体可增强IR-ET-1的分泌。已知的血管收缩肽，血管紧张素II（Ang II）和精氨酸加压素（AVP）可剂量依赖性地刺激内皮细胞分泌IR-ET-1。血管紧张素和加压素诱导的IR-ET-1产生被其各自的受体拮抗剂[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]完全抑制。结果表明，在具有特异性血管紧张素II和精氨酸加压素受体的内皮细胞中，肽刺激的IR-ET-1分泌是由受体介导的。这些发现首次证明了人脑毛细血管和微血管内皮细胞可产生IR-ET-1。
