Ca2+ signalling in mouse urethral smooth muscle in situ: role of Ca2+ stores and Ca2+ influx mechanisms

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp12837-list-0001">Contraction of urethral smooth muscle cells (USMCs) contributes to urinary continence. Ca²⁺ signalling in USMCs was investigated in intact urethral muscles using a genetically encoded Ca²⁺ sensor, GCaMP3, expressed selectively in USMCs.USMCs were spontaneously active in situ, firing intracellular Ca²⁺ waves that were asynchronous at different sites within cells and between adjacent cells.Spontaneous Ca²⁺ waves in USMCs were myogenic but enhanced by adrenergic or purinergic agonists and decreased by nitric oxide.Ca²⁺ waves arose from inositol trisphosphate type 1 receptors and ryanodine receptors, and Ca²⁺ influx by store‐operated calcium entry was required to maintain Ca²⁺ release events.Ca²⁺ release and development of Ca²⁺ waves appear to be the primary source of Ca²⁺ for excitation–contraction coupling in the mouse urethra, and no evidence was found that voltage‐dependent Ca²⁺ entry via L‐type or T‐type channels was required for responses to α adrenergic responses.