The microvasculature plays a primary role in the interchange of substances between tissues and the circulation. In visceral organs that undergo considerable distension upon filling, the microvasculature appears to display intrinsic contractile properties to maintain their flow. Submucosal venules in the bladder or gastrointestinal tract generate rhythmic spontaneous phasic constrictions and associated Ca2+ transients. These events are initiated within either venular pericytes or smooth muscle cells (SMCs) arising from spontaneous Ca2+ release from the sarcoplasmic reticulum (SR) and the opening of Ca2+-activated chloride channels (CaCCs) that trigger Ca2+ influx through L-type voltage-dependent Ca2+ channels (VDCCs). L-type VDCCs also play a critical role in maintaining synchrony within the contractile mural cells. In the stomach myenteric layer, spontaneous Ca2+ transients originating in capillary pericytes appear to spread to their neighbouring arteriolar SMCs. Capillary Ca2+ transients primarily rely on SR Ca2+ release, but also require Ca2+ influx through T-type VDCCs for their synchrony. The opening of T-type VDCCs also contribute to the propagation of Ca2+ transients into SMCs. In visceral microvasculature, pericytes act as either spontaneously active contractile machinery of the venules or as pacemaker cells generating synchronous Ca2+ transients that drive spontaneous contractions in upstream arterioles. Thus pericytes play different roles in different vascular beds in a manner that may well depend on the selective expression of T-type and L-type Ca2+ channels.