During the purinergic chemical transmission, neurons, neuroendocrine cells, glial cells, immune cells and other types of cells secrete ATP, and communicate with each other through purinoceptors on the plasma membrane. In spite of well-understood features on the signaling cascade after stimulation of the purinoreceptors, the mechanism of how ATP is stored and released from the purinergic cells is far less characterized. In this study, we focus on the mechanism on vesicular secretion through vesicular nucleotide transporter (VNUT). VNUT transports nucleotides such as ATP and ADP and plays an essential role in the vesicular storage and secretion of ATP. Recently, we identified the clinically available VNUT inhibitor clodronate, which impaired vesicular ATP release from neurons, microglia, and neutrophils. Clodronate also impaired neutrophil migration and attenuated neuropathic and inflammatory pain in vivo. Although more extensive works will be necessary, these studies show that VNUT-specific inhibitor is able to control vesicular ATP release in vivo and that VNUT regulates purinergic chemical transmission.