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Effect of nitric oxide on local vascular regulation in vivo perfusion system of rat.

一氧化氮对大鼠体内灌注系统局部血管调节的影响。

基本信息

批准号：
10670051
负责人：
HAYASHIDA Yoshiaki
金额：
$ 2.05万
依托单位：
University of Occupational and Environmental Health
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 2000
项目状态：
已结题

项目摘要

1) We improved nitric oxide (NO) measuring system in the vascular perfusion of rat. NO was measured with NO direct-measuring systems (Model No.501, or Model MES-100) with each NO selective electrode. A calibration curve was prepared for each electrode in both Models using an NO standard solution. The electrodes detected more than 0.06 nmole of NO.2) Acetylcholine (ACh) dose-dependently produced NO and concomitant vasodilation in the system. NO synthase inhibitor blocked NO release, but the vasodilation by ACh remained. The decrease in perfusion pressure (PP) in response to ACh was almost abolished in the presence of both L-NMMA and TEA or with deendothelialization. Bradykinin (BK) also induced NO release and biphasic effects on PP, which decreased with a lower concentration of BK and increased with a higher concentration. L-NMMA and TEA each abolished the decrease in PP induced by BK.In the presence of both L-NMMA and TEA, PP increased in response to BK.These results suggest that ACh and BK induce vasodilation through NO release and potassium channel dependent mechanism via endothelium.3) NO release by vasoconstriction in response to norepinephrine (NE) was investigated using this system in a model of hypertension (SHR) and normal control (WKY) rats between 4 and 16-week age. We found a significant correlation between NO release and the increase in PP by vasoconstriction in WKY between 4 and 16-week age, but not in age-matched SHR.NOx excretion in WKY was greater at 4-week age than that in age-matched SHR, and gradually decreased with aging from 4 to 16-week age. Whereas, NOx excretion in SHR did not change from 4 to 12-week age, and then decreased at 16-week age to a level of that in age-matched WKY.These results show that NO release decreased with age in both WKY and SHR, and suggest that there might be abnormal endothelial function of NO production to vasoconstriction in SHR.

1）我们改进了大鼠血管灌注一氧化氮（NO）测量系统。 NO 通过 NO 直接测量系统（型号 No.501 或型号 MES-100）和每个 NO 选择性电极进行测量。使用 NO 标准溶液为两个模型中的每个电极准备校准曲线。电极检测到超过 0.06 nmole 的 NO。2) 乙酰胆碱 (ACh) 在系统中剂量依赖性地产生 NO 并伴随血管舒张。 NO合酶抑制剂阻断NO释放，但ACh的血管舒张作用仍然存在。在 L-NMMA 和 TEA 存在或去内皮化的情况下，ACh 引起的灌注压 (PP) 降低几乎被消除。缓激肽 (BK) 还诱导 NO 释放和对 PP 的双相效应，随着 BK 浓度的降低而降低，随着浓度的升高而增加。 L-NMMA 和 TEA 各自消除了 BK 诱导的 PP 降低。在 L-NMMA 和 TEA 存在的情况下，PP 响应 BK 增加。这些结果表明，ACh 和 BK 通过内皮细胞的 NO 释放和钾通道依赖性机制诱导血管舒张。3) 使用该系统在高血压 (SHR) 和正常模型中研究了血管收缩响应去甲肾上腺素 (NE) 导致的 NO 释放 4 至 16 周龄的对照 (WKY) 大鼠。我们发现，在 4 至 16 周龄期间，WKY 中 NO 的释放与血管收缩引起的 PP 增加之间存在显着相关性，但在年龄匹配的 SHR 中则不然。WKY 中的 NOx 排泄量在 4 周龄时高于年龄匹配的 SHR，并且从 4 周龄到 16 周龄，NOx 排泄量逐渐减少。而SHR的NOx排泄量从4周龄到12周龄没有变化，然后在16周龄时下降到与WKY年龄匹配的水平。这些结果表明，WKY和SHR的NO释放量都随着年龄的增长而减少，这表明SHR中可能存在NO产生导致血管收缩的内皮功能异常。