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

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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.