Endothelium-derived relaxing factor contributes to the regulation of endothelial permeability.
Endothelium-derived relaxing factor contributes to the regulation of endothelial permeability.
复制标题
内皮源性舒张因子有助于内皮通透性的调节。
DOI：
10.1002/jcp.1041510309
复制
发表时间：
1992
影响因子：
5.6
通讯作者：
Oliver,JA
中科院分区：
文献类型：
--
作者：
Oliver,JA
To determine whether endothelium‐derived relaxing factor (EDRF) contributes to the regulation of endothelial permeability, the transendothelial flux of14C‐su‐crose, a marker for the paracellular pathway across endothelial monolayers (Oliver,J. Cell. Physiol.145:536–548, 1990), was examined in monolayers of bovine aortic endothelial cells grown on collagen‐coated filters. The permeability coefficient of14C‐sucrose was significantly decreased by 10−3M 8‐Bromoguanosine 3′,5′‐cyclic monophosphate or by 5 × 10−6M glyceryl trinitrate, an activator of soluble guanylate cyclase. Depletion of L‐arginine from endothelial monolayers increased14C‐sucrose permeability from 3.21 ± 0.59 to 3.88 ± 0.50 × 10−5cm · sec−1(mean ± SEM; n = 6;P< 0.05). The acute administration of 5 × 10−4M L‐arginine to monolayers depleted of this amino acid decreased14C‐sucrose permeability from 2.91 ± 0.27 to 2.52 ± 0.26 × 10−5cm · sec−1(n = 11;P< 0.05).14C‐sucrose permeability was increased by 10−7M bradykinin and this effect was enhanced by the presence of each one of the following compounds: 10−5M methylene blue, 4 × 10−6M oxyhemoglobin, 5 × 10−4M NG‐methyl‐L‐arginine or 5 × 10−4M Nω‐nitro‐L‐arginine. These results suggest that EDRF contributes to the sealing of the endothelial monolayer and that EDRF released by bradykinin acts as a feedback inhibitor attenuating the increase in endothelial permeability induced by this peptide. Because endothelial cells have the ability to contract and relax and possess guanylate cyclase responsive to nitric oxide, our results suggest that EDRF decreases14C‐sucrose permeability by relaxing endothelial cells, thereby narrowing the width of endothelial junctions. © 1992 Wiley‐Liss, Inc.
