Physiological and pathophysiological roles of endothelium-derived hyperpotarizing factor in the control of organ perfusion.

内皮衍生的高钾因子在器官灌注控制中的生理和病理生理作用。

• 批准号: 07307010
• 负责人: TAKESHITA Akira
• 金额: $ 6.21万
• 依托单位: KYUSHU UNIVERSITY FACULTY OF MEDICINE
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (A)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1997
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07307010/
• 关键词: EDHF; K channels; Nitric oxide; Microvessels; 血管内皮; 内皮由来過分極因子(EDHF); 一酸化窒素(NO); 内皮依存性弛緩反応; 内皮由来過分極因子; 血管平滑筋; EDHF; K channels; Nitric oxide; Microvessels; 血管内皮; 内皮由来過分極因子(EDHF); 一酸化窒素(NO); 内皮依存性弛緩反応; 内皮由来過分極因子; 血管平滑筋

1.Kanno et al. They found that acetylcholine-induced hyperpolarization is significantly reduced in streptozocin-induced diabetic rats and that lysophosphatidylcholine (LPC) impairs endothelium-dependent hyperpolarization in rats.2.Suzuki et al. They demonstrated that EDHF activates two Ca^<2+>-activated K-channels in the guinea-pig arteriole and that endothelium-dependent hyperpolarizations are achieved by both EDHF and prostanoids in the guinea-pig coronary artery.3.Itoh et al. They found that acetylcholine causes hyperpolarization via apaminsensitive K-channel in the rabbit middle cerebral artery and that non NO component largely contribute to the endothelium-dependent relaxation in rabbit microvessels.4.Yui et al. They revealed that LPC inhibits endothelium-dependent hyperpolarization and non NO-and non PG12-dependent relaxations in the porcine coronary artery.5.Shimokawa, Takeshita et al. They demonstrated that the importance of EDHF increases as the vessel size decreases in rats, rabbit, pigs, and humans and that estrogen and eicosapentaenoic acid improve both NO-mediated and EDHF-mediated relaxations in humans.6.Fuji et al. They found that EDHF-mediated relaxations are reduced in spontaneously hypertensive rats (SHR) and that antihypertensive therapy, especially that with ACE inhibitors, improves the reduced responses in SHR.7.Nakashima et al. They demonstrated that most of the inhaled anesthetics impair the EDHF-mediated relaxations and that vasoactive intestinal polypeptide may not be EDHF.

1.Kanno等。他们发现，乙酰胆碱诱导的超极化显着降低了链霉菌蛋白诱导的糖尿病大鼠，而溶血磷脂酰胆碱（LPC）损害了大鼠内皮依赖性超极化。2.Suzuki等。他们证明，EDHF激活了豚鼠动脉中的两个Ca^<2+>激活的K通道，并且在豚鼠冠状动脉中EDHF和前列腺素可以实现内皮依赖性超极化。他们发现，乙酰胆碱通过兔中大脑中动脉中的Apaminsensistive K通道引起超极化，而非成分在很大程度上有助于兔微型固定中的内皮依赖性弛豫。4.4.yui等。他们透露，LPC抑制猪冠状动脉中的内皮依赖性超极化和非PG12依赖性弛豫。5.shimokawa，Takeshita等。他们证明，随着老鼠，兔子，猪和人的血管尺寸的减小，EDHF的重要性增加，并且雌激素和eicosapentaenoic酸改善了人类的无介导和EDHF介导的放松。6.Fuji等人。他们发现，自发性高血压大鼠（SHR）中EDHF介导的弛豫减少，降压治疗，尤其是使用ACE抑制剂，可以改善SHR.7.nakashima等人的反应减少。他们证明，大多数吸入的麻醉药会损害EDHF介导的放松，并且血管活性肠多肽可能不是EDHF。