Calcium signaling in vascular smooth muscle is crucial for arterial tone regulation and vascular function. Several proteins, including Ca²⁺ channels, function in an orchestrated fashion so that blood vessels can sense and respond to physiological stimuli such as changes in intravascular pressure. Activation of the voltage-dependent Ca²⁺ channel, Cav1.2, leads to Ca²⁺ influx and consequently arterial tone development and vasoconstriction. Unique among Ca²⁺ channels, the vascular Cav3.2 T-type channel mediates feedback inhibition of arterial tone—and therefore causes vasodilation—of resistance arteries by virtue of functional association with hyperpolarizing ion channels. During aging, several signaling modalities are altered along with vascular remodeling. There is a growing appreciation of how calcium channel signaling alters with aging and how this may affect vascular function. Here, we discuss key determinants of arterial tone development and the crucial involvement of Ca²⁺ channels. We next provide an updated view of key changes in Ca²⁺ channel expression and function during aging and how these affect vascular function. Further, this article synthesizes new questions in light of recent developments. We hope that these questions will outline a roadmap for new research, which, undoubtedly, will unravel a more comprehensive picture of arterial tone dysfunction during aging.

血管平滑肌中的钙信号对动脉张力调节和血管功能至关重要。包括 Ca ²⁺通道在内的几种蛋白质以协调的方式发挥作用，因此血管可以感知生理刺激并对其做出反应，例如血管内压的变化。电压依赖性 Ca ²⁺通道 Cav1.2 的激活导致 Ca ²⁺内流，从而导致动脉张力发展和血管收缩。^{在 Ca 2+}中独一无二通道，血管 Cav3.2 T 型通道通过与超极化离子通道的功能关联介导动脉张力的反馈抑制，从而导致阻力动脉的血管舒张。在衰老过程中，几种信号传导方式随着血管重塑而改变。人们越来越了解钙通道信号如何随着衰老而改变，以及这如何影响血管功能。在这里，我们讨论动脉张力发展的关键决定因素和 Ca ²⁺通道的关键参与。我们接下来提供 Ca ^{2+关键变化的更新视图}通道在衰老过程中的表达和功能以及这些如何影响血管功能。此外，本文根据最近的发展综合了新问题。我们希望这些问题能够勾勒出新研究的路线图，毫无疑问，这将揭示衰老过程中动脉张力功能障碍的更全面图景。