Urine expulsion from the upper urinary tract is a necessary process that eliminates waste, promotes renal filtration, and prevents nephron damage. To facilitate the movement of urine boluses throughout the upper urinary tract, smooth muscle cells that line the renal pelvis contract in a coordinated effort to form peristaltic waves. Resident pacemaker cells in the renal pelvis are critical to this process and spontaneously evoke transient depolarizations that initiate each peristaltic wave and establish rhythmic contractions. This talk will discuss the mechanisms responsible for pacemaking and our current methods to improve the identification of pacemaker cells. Until recently, renal pacemakers have been termed "atypical smooth muscle cells" due to their low expression of smooth muscle myosin and poor organization of myofilaments compared to "typical smooth muscle cells" that perform peristalsis. Our group discovered that pacemaker cells also express the tyrosine kinase receptor PDGFRα, enabling their identification and purification amongst other renal pelvis cell types. Employing our improved identification methods, we have determined that the calcium-activated chloride channel, ANO1, is expressed by pacemaker cells and may contribute to spontaneous depolarization. A greater understanding of pacemaker and peristaltic mechanisms is warranted since aberrant contractile function may underlie diseases such as hydronephrosis, a deleterious condition that can cause significant and irreversible nephron damage.