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. 2018 Dec 4;9:1389. doi: 10.3389/fphar.2018.01389

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Copyright © 2018 She, Ma, Liu, Zhang, Qiu, Chen, Li, Xue, Luo, Wang, Xu, Zang, Zhao, Cao, Shen, Peng, Zhao, Yu, Chen, Nie, Shen, Chen, Chen, Qin, Dai, Chen and Liu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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EESC via inhibiting ion channel-mediated Ca²⁺ influx inhibits ACh-induced contraction. (A) A TR was contracted by ACh, and the contraction was inhibited by nifedipine and then blocked by EESC. (B) The contraction was reduced by nifedipine and then blocked by YM-58483. (C) In the presence of nifedipine, ACh induced a transient contraction in Ca²⁺-free conditions (0 Ca²⁺ and 0.5 mM EGTA). After the addition of 2 mM Ca²⁺, a sustained contraction occurred, which was blocked by EESC. (D) These contractions were markedly inhibited in an EESC-incubated TR. Each of the above experiments was conducted in 6–8 TRs, and the same results were observed. These results demonstrate that EESC-induced relaxation is due to the inhibition of LVDCCs and other pathways.