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Regulation of vascular tone by endothelium, nerve and blood cells through their reciprocal actions.

内皮、神经和血细胞通过相互作用来调节血管张力。

基本信息

批准号：
03454371
负责人：
FUKUDA Satoru
金额：
$ 3.71万
依托单位：
Niigata University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1993
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-03454371/
关键词：
Hypoxia Endothlium Adventitia Calcium Vascular smooth muscle アシド-シス血管内皮

项目摘要

We investigated the effects of endothelium, adventitia (nerve), and blood cells(white blood cells : WBC) on vascular tone during hypoxia or acidosis. Hypoxia contracted blood vessels. Removal of endothelium attenuated the hypoxia-induced contraction of blood vessels. Cyclooxygenase inhibitors attenuated the hypoxia-induced contraction of blood vessels, suggesting that cyclooxygenase related eicosanoids may be released from endothlium during hypoxia. In contrast, removal of endothlium and adventitia abolished the hypoxia-induced contraction. These findings syggest that adventitia as well as endothlium may contribute to the hypoxia-induced contraction. It was also found that acidosis attnuated the agonist-induced contraction in a different manner depending the type of agonists used, and that endothelium facilitated the attenuated action of acidosis on agonist-induced contraction. From the experiment concerning the effect of WBC on vascular tone, we found that WBC dilates vascular smooth muscle indirectly through endothlium. We investigated the substance released from endothelium using some kinds of antagonists. However, we could not detect the substance. It has been reported that shear stress on endothelium releases endothlium-derived relaxing substance(s). Applying these phenomenon to research in testing human endothelial function, we found that endothelium did not work well in some kind of disease. In summary we found that endothelium, adventitia and blood vessels regulate vascular tone through their reciprocal actions.

我们研究了缺氧或酸中毒期间内皮、外膜（神经）和血细胞（白色血细胞：WBC）对血管张力的影响。缺氧使血管收缩。去除内皮可减弱缺氧引起的血管收缩。环氧合酶抑制剂可减弱缺氧引起的血管收缩，提示缺氧时内皮细胞可能释放环氧合酶相关的类花生酸。相反，去除内皮细胞和外膜则可消除缺氧引起的收缩。这些结果提示，外膜和内皮细胞都参与了缺氧引起的收缩。还发现，酸中毒attnuated激动剂诱导的收缩，以不同的方式依赖于所使用的激动剂的类型，和内皮细胞促进酸中毒对激动剂诱导的收缩的衰减作用。从白细胞对血管张力影响的实验中发现，白细胞通过内皮细胞间接扩张血管平滑肌。我们用几种拮抗剂研究了内皮细胞释放的物质。但是，我们无法检测到该物质。据报道，内皮上的剪切应力释放内皮源性舒张物质。将这些现象应用于检测人体内皮功能的研究中，发现内皮在某些疾病中并不起作用。总之，我们发现内皮、外膜和血管通过它们的相互作用调节血管张力。