The pyeloureteral function is to transport urine from the kidneys into the ureter toward the urinary bladder for storage until micturition. A set of mechanisms collaborates to achieve this purpose: the basic process regulating ureteral peristalsis is myogenic, initiated by active pacemaker cells located in the renal pelvis. Great emphasis has been given to hydrodynamic factors, such as urine flow rate in determining the size and pattern of urine boluses which, in turn, affect the mechanical aspects of peristaltic rhythm, rate, amplitude, and baseline pressure. Neurogenic contribution is thought to be limited to play a modulatory role in ureteral peristalsis. The myogenic theory of ureteral peristalsis can be traced back to Engelmann (1) who was able to localize the peristaltic pressure wave's origin in the renal pelvis and suggested that the ureteral contraction impulse passes from one ureteral cell to another, the whole ureter working as a functional syncitium. Recent studies of ureteral biomechanics, smooth muscle cell electrophysiology, membrane ionic currents, cytoskeletal components and pharmacophysiology much improved our understanding of the mechanism of how the urine bolus is propelled, how this process is disturbed in pathological states, and what could be done to improve it.