Coordinating blood flow to active tissue requires vasomotor responses to conduct among resistance arteries. Vasomotor spread is governed by the electrical and mechanical properties of vessels; the latter being linked to the sigmoid relations between membrane potential (V_M), [Ca²⁺], and smooth muscle contractility. Proteins guiding electrical-to-tone translation are subject to regulation; thus, vasomotor conduction could be viewed as "pliant" to the current regulatory state. Using simple in silico approaches, we explored vasomotor pliancy and how the regulation of contractility impacts conduction along a skeletal muscle artery and a branching cerebrovascular network. Initial simulations revealed how limited electromechanical linearity affects the translation of electrical spread into arterial tone. Subtle changes to the V_M-[Ca²⁺] or [Ca²⁺]-diameter relationship, akin to regulatory alterations in Ca²⁺ influx and Ca²⁺ sensitivity, modified the distance and amplitude of the conducted vasomotor response. Simultaneous changes to both relationships, consistent with agonist stimulation, augmented conduction although the effect varied with stimulus strength and polarity (depolarization vs hyperpolarization). Final simulations using our cerebrovascular network revealed how localized changes to the V_M-[Ca²⁺] or [Ca²⁺]-diameter relationships could regionally shape conduction without interfering with the electrical spread. We conclude that regulatory changes to key effector proteins (e.g. L-type Ca²⁺ channels, myosin light chain phosphatase), integral to voltage translation, not only impact conducted vasomotor tone but likely blood flow delivery to active tissues.

中文翻译：

---

将传导概念化为柔韧的血管舒缩反应：Ca2+ 通量和 Ca2+ 敏化的影响。


协调流向活动组织的血流需要血管舒缩反应在阻力动脉之间进行。血管舒缩扩散受血管的电气和机械特性控制；后者与膜电位 (V _M )、[Ca ²⁺ ] 和平滑肌收缩力之间的 S 形关系有关。指导电到音调翻译的蛋白质受到监管；因此，血管舒缩传导可以被视为“顺从”当前的监管状态。使用简单的计算机方法，我们探索了血管舒缩柔韧性以及收缩性的调节如何影响沿骨骼肌动脉和分支脑血管网络的传导。初步模拟揭示了有限的机电线性如何影响电传播到动脉张力的转换。 _VM -[Ca ²⁺ ] 或[Ca ²⁺ ]-直径关系的微妙变化，类似于Ca ²⁺流入和Ca ²⁺敏感性的调节变化，改变了所进行的血管舒缩反应的距离和幅度。两种关系同时发生变化，与激动剂刺激一致，增强传导，尽管效果随刺激强度和极性（去极化与超极化）而变化。使用我们的脑血管网络进行的最终模拟揭示了_VM -[Ca ²⁺ ] 或 [Ca ²⁺ ] 直径关系的局部变化如何在不干扰电传播的情况下局部塑造传导。我们得出的结论是，关键效应蛋白的监管发生了变化（例如 L 型 Ca ²⁺通道（肌球蛋白轻链磷酸酶）是电压转换的组成部分，不仅影响传导的血管舒缩张力，还可能影响向活动组织的血流输送。