In microvascular of visceral organs, such as the bladder and gut, α-smooth muscle actin negative, non-contractile pericytes in capillaries periodically generate spontaneous Ca²⁺ transients. The spontaneous Ca²⁺ transients are not only synchronously developed amongst a network of capillary pericytes but also capable of propagating upstream to contractile pericytes in precapillary arterioles and thereby regulate capillary perfusion. The capillary pericytes express ANO1 Ca²⁺-activated chloride channels and generate ANO1-dependent spontaneous transient inward currents and corresponding spontaneous transient depolarisations (STDs). Both spontaneous Ca²⁺ transients and STDs primarily arise from a cycle of spontaneous Ca²⁺ release and uptake through sarcoplasmic reticulum (SR) Ca²⁺ stores that is maintained by Ca²⁺ influx via Orai channels, while neither L- nor T-type voltage-dependent Ca²⁺ channels play a fundamental role. Thus, STDs arising from spontaneous Ca²⁺ transients serve as a means of intercellular communication where STDs appear to gain a regenerative nature depending on depolarisation-induced SR Ca²⁺ release, presumably via InsP₃ production.