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。

基本信息

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

项目摘要

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.菅野等人。他们发现，在链佐星诱导的糖尿病大鼠中，乙酰胆碱诱导的超极化显着降低，并且溶血磷脂酰胆碱（LPC）会损害大鼠内皮依赖性超极化。2.Suzuki 等人。他们证明EDHF激活豚鼠小动脉中的两个Ca 2+ 激活的K通道，并且EDHF和前列腺素类药物在豚鼠冠状动脉中实现内皮依赖性超极化。 3.Itoh等人。他们发现乙酰胆碱通过对兔大脑中动脉的apamin敏感的K通道引起超极化，而非NO成分很大程度上有助于兔微血管的内皮依赖性舒张。4.Yui等人。他们发现，LPC 抑制猪冠状动脉内皮依赖性超极化以及非 NO 和非 PG12 依赖性舒张。 5. Shimokawa，Takeshita 等人。他们证明，在大鼠、兔、猪和人类中，EDHF 的重要性随着血管尺寸的减小而增加，并且雌激素和二十碳五烯酸可以改善人类中 NO 介导的和 EDHF 介导的松弛。 6.Fuji 等人。他们发现自发性高血压大鼠 (SHR) 中 EDHF 介导的松弛现象减少，而抗高血压治疗，尤其是 ACE 抑制剂，可改善 SHR 中减少的反应。7.Nakashima 等人。他们证明，大多数吸入麻醉剂都会损害 EDHF 介导的松弛，并且血管活性肠多肽可能不是 EDHF。