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

1.Kanno等人。他们发现，在链脲佐菌素诱导的糖尿病大鼠中，乙酰胆碱诱导的超极化显著减少，溶血磷脂酰胆碱(LPC)损害了大鼠的内皮依赖性超极化。他们证实，EDHF激活豚鼠小动脉上两个钙激活的K通道，EDHF和前列腺素都能实现豚鼠冠状动脉内皮依赖性超极化。他们发现乙酰胆碱通过氨基敏感的K通道引起兔大脑中动脉的超极化，并且非NO组分在很大程度上参与了兔微血管的内皮依赖性松弛。他们发现LPC抑制猪冠状动脉内皮依赖的超极化以及非NO和非PG12依赖的松弛。他们证明，在大鼠、兔、猪和人类中，随着血管大小的减小，EDHF的重要性增加，雌激素和二十碳五烯酸改善了NO介导的和EDHF介导的人体松弛。他们发现EDHF介导的松弛在自发性高血压大鼠(SHR)中减少，抗高血压治疗，特别是使用ACE抑制剂的治疗，改善了SHR中减少的反应。他们证明，大多数吸入麻醉药损害了EDHF介导的松弛，血管活性肠肽可能不是EDHF。

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.