权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

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. Kanno等人发现，乙酰胆碱诱导的超极化在链脲佐菌素诱导的糖尿病大鼠中显著降低，溶血磷脂酰胆碱（LPC）损害大鼠的内皮依赖性超极化。2. Suzuki等人证明，EDHF激活豚鼠小动脉中的两个Ca^<2+>激活的K通道，并且豚鼠小动脉中的内皮依赖性超极化通过EDHF和前列腺素类实现。猪冠状动脉。3. Itoh等。他们发现乙酰胆碱通过兔大脑中动脉中的apaminsensitive K通道引起超极化，而非NO组分在很大程度上有助于兔微血管的内皮依赖性舒张。4. Yui等。他们揭示LPC抑制内皮依赖性超极化，而非NO和非PG 12- 5. Shimokawa，Takeshita等，他们证明了EDHF的重要性随着大鼠、兔、猪和人类，雌激素和二十碳五烯酸改善NO介导的和EDHF介导的松弛作用。6. Fuji等，他们发现EDHF-在自发性高血压大鼠（SHR）中，EDHF介导的舒张功能降低，抗高血压治疗，特别是ACE抑制剂，改善了SHR中降低的反应。7. Nakashima等，他们证明大多数吸入麻醉剂损害EDHF介导的舒张功能，并且血管活性肠多肽可能不是EDHF。