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. 2020 Apr 4;56:1–18. doi: 10.1540/jsmr.56.1

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©2020 The Japan Society of Smooth Muscle Research

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives (by-nc-nd) License. (CC-BY-NC-ND 4.0: http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 3. — Proposed mechanisms underlying synchronous spontaneous Ca²⁺ transients in mural cells.

A: Spontaneous Ca²⁺ release from sarco-endoplasmic reticulum (SR/ER) via IP₃ receptors (IP₃R) and/or ryanodine receptors (RyR) triggers the opening of Ca²⁺-activated Cl^- channels (CaCCs) to depolarise the membrane (ΔV) (cf. reference 41). The CaCC-dependent depolarisation further activates voltage-dependent Ca²⁺ channels (VDCCs). Ca²⁺ influx through VDCCs stimulates Ca²⁺-induced Ca²⁺ release (CICR) via RyR and/or IP₃R, and CaCC-dependent membrane depolarisation (ΔV) would increase IP₃ production to facilitate IP₃-induced Ca²⁺ release. The sequestration of cytosolic Ca²⁺ is mediated by sarco-endoplasmic reticulum Ca²⁺-ATPase (SERCA). B: In a rat bladder suburothelial venule, individual spontaneous action potentials of venular smooth muscle cells (upper trace) precede each vasoconstriction as shown by a reduction in venular diameter (lower trace). Traces in B are reproduced from (38) with permission.