Effective And Mechanism Of ACh-induced Constriction In Umbilical Cord Vessels

OBJECTIVE To determine mechanisms of Acetylcholine(ACh)-mediated human umbilical vasoconstrictions.METHODS This study used umbilical veins and arteries from pregnant women (n=85), also used veins and arteries from rat and sheep umbilical, as well as aortas,mesentery arteries from rats, fetal mesentery, carotid and femoral arteries from sheep, to compare vascular functions among different vessels, and to determine the mechanisms of ACh-mediated vasoconstriction in human umbilical.RESULTS The results showed that ACh caused dramatic vasoconstriction in HUA and HUV, rat, and sheep without significant vasodilatation effects, In addition, ACh-induced constriction in umbilical was not only in rest status, but also in tension status generated by other vascular stimulators. ACh did not show constriction in all other vessels, including fetal vessels. Administration of atropine (10-5M) inhibited the effect of ACh. The mRNA of M1-M5receptor subtypes were expressed in human umbilical vessels. Signal of Protein kinase C(PKC) antagonist GF109203X hydrochloride (GF,10-5M), or calcium inhibitor nifidipine (10-5M) decreased vasoconstriction by ACh in umbilical. ACh also caused reduction of whole cell potassium(K+) channel currents and single channel current of BKca2+(Calcium-activated potassium channel).CONCLUSIONS The results suggested that umbilical vessels were significantly different from other vessels in response to ACh, and provided novel information that is important to obstetrics and fetology because umbilical vessels play critical roles in supply of nutritions and oxygen for fetuses.