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Muscarinic‐mediated vasoconstriction in human, rat and sheep umbilical cords and related vasoconstriction mechanisms
Author(s) -
Chen N,
Lv J,
Bo L,
Li N,
Wu C,
Yin X,
Li J,
Tao J,
Chen J,
He Y,
Huang S,
Xiao J,
Mao C,
Xu Z
Publication year - 2015
Publication title -
bjog: an international journal of obstetrics and gynaecology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.157
H-Index - 164
eISSN - 1471-0528
pISSN - 1470-0328
DOI - 10.1111/1471-0528.13144
Subject(s) - vasoconstriction , umbilical cord , vasodilation , umbilical artery , endocrinology , medicine , mesenteric arteries , umbilical vein , vascular smooth muscle , muscarinic acetylcholine receptor , fetus , anatomy , biology , artery , receptor , pregnancy , biochemistry , genetics , smooth muscle , in vitro
Objective The umbilical cord provides nutrition and oxygen to the fetus. The aim of this study was to determine the effects of acetylcholine ( AC h) on umbilical cords from humans and other mammals, and the mechanisms of AC h‐mediated vasoconstriction in the human umbilical cord. Design Human and animal umbilical cords used in vascular and cellular experiments. Setting Institute for Fetology, First Hospital of Soochow University, Suzhou, China. Population A total of 85 pregnant women, 16 Sprague Dawley rats and seven pregnant sheep. Methods Umbilical cord veins and arteries from humans, rats and sheep, aortas and mesenteric arteries from rats, and mesenteric, carotid and femoral arteries from ovine fetuses were used to compare vascular functions in response to AC h and to determine the mechanisms of AC h‐mediated umbilical vasoconstriction. Vascular tension and ion channel currents were measured on isolated vessels and smooth muscle cells from human umbilical cords. Main outcome measures Provision of new evidence to conclude that AC h‐stimulated vasoconstriction is common to all umbilical cords, and cellular mechanisms are linked to potassium channels. Results ACh caused reliable vasoconstriction in umbilical veins/arteries in humans, rats and sheep, but not in any other vessels, including fetal vessels. Atropine inhibited the effects of ACh. The m RNA of ACh‐muscarinic receptor subtypes M 1 –M 5 was expressed in human umbilical vessels. The protein kinase C antagonist GF109203X and the calcium inhibitor nifedipine decreased ACh‐induced vasoconstriction in human umbilical vessels. ACh also caused a reduction in whole‐cell potassium channel currents and the single‐channel current of large‐conductance calcium‐activated potassium (BKca) channels. Conclusion Umbilical vessels are significantly different from other vessels in their response to AC h. BK ca channels in smooth muscle cells may play important roles in AC h‐mediated vasoconstriction in human umbilical cords. This information may be important for fetal medicine and practice with regard to the effect on fetal development of umbilical vascular functions.