Spontaneous rhythmic constrictions known as vasomotion are developed in several microvascular beds in vivo. Vasomotion in arterioles is considered to facilitate blood flow, while venular vasomotion would facilitate tissue metabolite drainage. Mechanisms underlying vasomotion periodically generate synchronous Ca²⁺ transients in vascular smooth muscle cells (VSMCs). In visceral organs, mural cells (pericytes and VSMCs) in arterioles, capillaries and venules exhibit synchronous spontaneous Ca²⁺ transients. Since sympathetic regulation is rather limited in the intra-organ microvessels, spontaneous activity of mural cells may play an essential role in maintaining tissue perfusion. Synchronous spontaneous Ca²⁺ transients in precapillary arterioles (PCAs)/capillaries appear to propagate to upstream arterioles to drive their vasomotion, while venules develop their own synchronous Ca²⁺ transients and associated vasomotion. Spontaneous Ca²⁺ transients of mural cells primarily arise from IP₃ and/or ryanodine receptor-mediated Ca²⁺ release from sarcoendoplasmic reticulum (SR/ER) Ca²⁺ stores. The resultant opening of Ca²⁺-activated Cl^- channels (CaCCs) causes a membrane depolarisation that triggers Ca²⁺ influx via T-type and/or L-type voltage-dependent Ca²⁺ channels (VDCCs). Mural cells are electrically coupled with each other via gap junctions, and thus allow the sequential spread of CaCC or VDCC-dependent depolarisations to develop the synchrony of Ca²⁺ transients within their network. Importantly, the synchrony of spontaneous Ca²⁺ transients also requires a certain range of the resting membrane potential that is maintained by the opening of K_v7 voltage-dependent K⁺ (K_v7) and inward rectifier K⁺ (K_ir) channels. Thus, a depolarised membrane would evoke asynchronous, ‘premature’ spontaneous Ca²⁺ transients, while a hyperpolarised membrane prevents any spontaneous activity.