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To clarify which endothelium derived vasodilators and K+ channels contribute to the vasodilation in arterioles of the guinea-pig choroids

阐明哪些内皮源性血管舒张剂和 K 通道有助于豚鼠脉络膜小动脉的血管舒张

基本信息

批准号：
10671651
负责人：
TOMIDA Kazuyuki
金额：
$ 1.92万
依托单位：
Nagoya City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

项目摘要

The purpose of this study is to clarify which endothelium-derived vasodilators and K+ channels contribute to the vasodilation in arterioles of the guinea-pig choroids. Experiment1 was done on acetylcholine (ACh)-induced vasodilation. The choroid was isolated from the guinea-pig eyeball, pinned flat on a silicone plate, and superfused with Kerbs solution. Diameters of choroidal arterioles were measured using video microscopy. In norepinephrine (NE, 1-5M)-constricted arterioles, the combination of nitroarginine(N-Arg, 10-4M) and indomethacin (Indo, 10-5M) reduced ACh (10-6M)-induced vasodilation by 24%. When high K+ solution was used to constrct the arterioles, ACh-induced vasodilation was abolished by N-Arg and Ind. In the presence of N-Arg and Ind, the ACh-induced dilation of NE-constricted arterioles was attenuated by tetraethylammonium(10-3M), apamin(10-7M) and charybdotoxin(ChTX, 10-7M) but not by glibenclamide(Glib, 2'10-5M). Simultaneous application of apamin and ChTX inhibited th … More e ACh-induced dilation by 85%. In arterioles of guinea-pig choroids, nitric oxide and prostacyclin are not main mediators in ACh-induced vasodilation. Simultaneous activation of a set of Ca2+-sensitive K+ channels may take most part of ACh-induced vasodilation. Experiment 2 was performed on NaCN-induced ischemic vasodilation. The guinea-pig choroid was prepared in the same way as experiment 1. Vasodilatory effects were examined after the choroid was exposed to glucose-free/NaCN solution solution for 10 minutes. N-Arg, Glib, and ChTX significantly inhibited glucose-free/NaCN-induced vasodilation by 47%, 62%, and 24%, respectively. No significant inhibitory effect was observed with Indo. Simultaneous application of Glib and ChTX reduced vasodilation by 77%. When Glib and ChTX were added together to N-Arg, dilation was reduced by 86%. With high K+ Krebs solution, ischemia caused a slight vasodilation(11%), which was significantly inhibited by N-Arg. Glucose-free/NaCN-induced ischemic vasodilation was mainly mediated by NO and KATP channels. A part of NO-mediated vasodilation was induced independent of the opening of K+ channels. Less

本研究的目的是阐明哪些内皮源性血管舒张剂和K+通道有助于豚鼠脉络膜小动脉的血管舒张。实验一为乙酰胆碱（ACh）引起的血管舒张反应。从豚鼠眼球中分离脉络膜，将其平放在硅胶板上，并用Kerbs溶液灌注。用视频显微镜测量脉络膜小动脉的直径。在去甲肾上腺素（NE，1- 5 M）收缩的小动脉中，硝基精氨酸（N-Arg，10- 4 M）和吲哚美辛（Indo，10- 5 M）的组合使ACh（10- 6 M）引起的血管舒张减少24%。当用高K+溶液收缩小动脉时，N-Arg和Ind可阻断ACh引起的血管舒张作用，而四乙基铵（10 ~（-3）M）、apamin（10 ~（-7）M）和Charybdotoxin（ChTX，10 ~（-7）M）可阻断ACh引起的NE收缩小动脉的血管舒张作用，格列本脲（Glib，2 '10 ~（-5）M）对ACh引起的NE收缩小动脉的血管舒张作用无影响。同时应用apamin和ChTX抑制了 ...更多信息 e乙酰胆碱诱导的扩张达85%。在豚鼠脉络膜微动脉中，一氧化氮和前列环素不是乙酰胆碱舒张血管的主要介质。同时激活一组Ca ~（2+）敏感的K ~+通道可能是ACh引起的血管舒张的主要原因。实验2是在NaCN诱导的缺血性血管舒张上进行的。以与实验1相同的方式制备豚鼠脉络膜。在脉络膜暴露于无葡萄糖/NaCN溶液溶液10分钟后检查血管舒张作用。N-Arg、Glib和ChTX分别显著抑制无葡萄糖/NaCN诱导的血管舒张47%、62%和24%。未观察到Indo的显著抑制作用。同时应用Glib和ChTX可使血管舒张减少77%。当将Glib和ChTX一起添加到N-Arg中时，扩张减少了86%。高K+ Krebs液缺血引起轻度血管舒张（11%），N-Arg可显著抑制血管舒张。无葡萄糖/NaCN诱导的缺血性血管舒张主要由NO和KATP通道介导。一部分NO介导的血管舒张作用不依赖于K+通道的开放。少