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OS 02-06 人动脉中细胞内ATP介导系统对血管运动的生理调节

OS 02-06 PHYSIOLOGICAL REGULATION OF VASOMOTION BY INTRACELLULAR ATP-MEDIATED SYSTEM IN HUMAN ARTERY.

作者信息

Kim Young Chul, Kim Dae Hoon, Lee Sang Eok, Kim Chan Hyung, Choi Woong, Lee Sang Jin, Yun Hyo-Yung

机构信息

1Department of Physiology, Chungbuk National University School of Medicine, Korea, Republic of 2Department of Surgery, Chungbuk National University School of Medicine, Korea, Republic of 3Department of Surgery, Konyang University, Korea, Republic of 4Department of Pharmacology, Chungbuk National University School of Medicine, Korea, Republic of.

出版信息

J Hypertens. 2016 Sep;34(Suppl 1-ISH 2016 Abstract Book):e49. doi: 10.1097/01.hjh.0000499981.55788.a6.

Abstract

OBJECTIVE

Spontaneous oscillation of tone of blood vessel called vasomotion cause vessel to flow blood which is an oscillation of flow into an organ. Microcirculation is sensitive to hypoxic condition and metabolism but mechanism of vasomotion is still poorly understood.

DESIGN AND METHOD

Purpose: We studied involvement of metabolism-mediated regulation by intracellular ATP level of vasomotion in human gastric artery.

METHODS

Conventional contractile measuring system and Western blot were used.

RESULTS

Circular muscle of human gastric artery produced sustained tonic contraction of 1.0 ± 0.19 g by 50 mM high K (n = 36). Pinacidil (10 μM), which is known to activatorof ATP-sensitive K (KATP) channel inhibited vasomotion completely in a reversible manner. Inhibition of vasomotion by activators of KATP channel recovered by glibenclamide. Diazoxide (300 μM), cromakalim (10 μM) nicorandil (10 μM) which is known to activate KATP channel also completely blocked vasomotion in a glibenclamide sensitive manner. Inhibitory effect of these openers of KATP channel on serotonin and norepinephrine-induced contraction were also recoded in a glibenclmide-sensitive manner. In human artery, glucose-free condition which is elated metabolic changes inhibited vasomotion and it was recovered by glibenclamide. Finally, molecular subtypes of KATP channel was defined by Western blot in human artery.

CONCLUSIONS

Vasomotion of human gastroepiploic artery was inhibited by activation of specific subtypes of KATP channel and alteration of metabolism.

摘要

目的

血管张力的自发振荡称为血管运动,它使血管内血液流动,这是一种流入器官的血流振荡。微循环对缺氧状态和代谢敏感,但血管运动的机制仍知之甚少。

设计与方法

目的:我们研究了人胃动脉中细胞内ATP水平介导的代谢调节对血管运动的影响。

方法

使用传统的收缩测量系统和蛋白质免疫印迹法。

结果

50 mM高钾使人类胃动脉环行肌产生1.0±0.19 g的持续强直性收缩(n = 36)。已知可激活ATP敏感性钾(KATP)通道的吡那地尔(10 μM)以可逆方式完全抑制血管运动。格列本脲可恢复KATP通道激活剂对血管运动的抑制作用。已知可激活KATP通道的二氮嗪(300 μM)、克罗卡林(10 μM)、尼可地尔(10 μM)也以格列本脲敏感的方式完全阻断血管运动。这些KATP通道开放剂对5-羟色胺和去甲肾上腺素诱导的收缩的抑制作用也以格列本脲敏感的方式记录下来。在人体动脉中,与代谢变化相关的无葡萄糖状态抑制血管运动,格列本脲可使其恢复。最后,通过蛋白质免疫印迹法确定了人体动脉中KATP通道的分子亚型。

结论

人胃网膜动脉的血管运动受到KATP通道特定亚型激活和代谢改变的抑制。

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