Journal
REPRODUCTIVE TOXICOLOGY
Volume 65, Issue -, Pages 95-103Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.reprotox.2016.07.003
Keywords
Acetylcholine; Umbilical cord; Calcium channel; Potassium channel
Categories
Funding
- NSFC [2012CB947600, 2013BAI04B05, 81070540, 81320108006, 81370719]
- Jiangsu Key Discipline/Laboratory Funds
- Jiangsu Key Discipline of Human Assisted Reproduction Medicine Funds
Ask authors/readers for more resources
We recently demonstrated that acetylcholine (ACh) produced reliable vasoconstrictions in the umbilical cords. This study investigated the possible mechanisms with different antagonists. ACh-mediated vasoconstrictions were decreased by voltage-operated calcium (Ca2+) channels antagonist nifedipine or inositol-1,4,5-trisphosphate-mediated Ca2+ release antagonist 2-aminoethyl diphenylborinate, indicating that both extracellular and intracellular calcium modulated the ACh-stimulated umbilical contraction. Intracellular Ca2+ concentrations were increased simultaneously with vasoconstrictions by ACh in the umbilical vessels. Inhibiting large-conductance calcium-dependent potassium (BK) channels enhanced ACh-mediated contraction, whereas inhibiting voltage dependent potassium (K+), inward rectifier K+ and ATP-sensitive K+ channels had no effects. Incubation with specific K+ channel inhibitors showed that ACh suppressed BK currents rather than 4-aminopyridine-sensitive K+ channels currents. The results suggested that blood vessels in umbilical cords had special characteristics in response to cholinergic signals. ACh-stimulated umbilical vasoconstrictions were mediated via muscarinic receptor subtype 1/3-protein kinase C/cyclooxygenase-BK channel pathways. (C) 2016 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available