Spontaneous activity in the microvasculature of visceral organs: Role of pericytes and voltage-dependent Ca²⁺ channels

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.