[Participation of neuropeptide Y Y3-receptor subtype in the increase in lung vascular permeability--for therapy of XXXX ].

@entity825 @entity3126 @entity2515 @entity4 @entity1942 @entity1576 @entity1063
In order to find some treatments for @entity1576 caused by @entity3126 , we investigated the mechanism of @entity3126 . Previously, stimulation of sympathetic nerves caused an increase in pulmonary vascular permeability, possibly due to neuropeptide Y. Neuropeptide Y injected into the @entity825 increased lung vascular permeability dose-dependently, the ED50 of which was 0.3-1 nM. Such an effect remained even after treatment with @entity2515 , as well as in the presence of alpha- and beta-blockers. And @entity1063 enhanced the effect of neuropeptide Y on lung vascular permeability. These responses were almost similar to those obtained by stimulation of sympathetic nerves. Furthermore, neuropeptide Y, in fibrin-induced @entity3126 , was localized in alveolar macrophages and alveolar spaces, amounting to approximately 200 nM in @entity4 fluid. The value was significantly greater than that obtained in hydrostatic @entity3126 by 10-30 times. @entity1942 , an analogue of neuropeptide Y, had no action on lung vascular permeability, whereas the effect of neuropeptide Y was inhibited by pretreatment with neuropeptide Y- 13-36, an antagonist for Y3-recetor subtype. These results suggested that neuropeptide Y enhances the lung vascular permeability via Y3-recetor subtype. Neuropeptide Y- 13-36, in fibrin-induced @entity3126 , decreased a ratio of protein concentration in @entity4 fluid to that in serum, indicating that neuropeptide Y actually acts a role in the development of @entity3126 , via an increase in lung vascular permeability.
