The smooth muscle organs of the lower urinary tract comprise the bladder detrusor smooth muscle (DSM) and internal urethral sphincter, which have a reciprocal contractile relationship during urine storage and micturition. As the bladder fills with urine, DSM remains relaxed to accommodate increases in intravesical pressure while urethral smooth muscle cells (USMC) generate sustained tone to occlude the urethral orifice, preventing leakage. Upon onset of micturition, this contractile behaviour reverses, as USMC relax, allowing passage of urine from the bladder, which contracts to expel urine via the now open urethra. While neither of these organs displays uniform coordinated regular contractions, similar to phasic tissues such as the small intestine, lymphatics or renal pelvis, they do exhibit certain patterns of rhythmicity at cellular and tissue levels which underly their physiological function. In rabbit and guinea-pig urethra, regular electrical slow waves are recorded from circular USMC. This activity is linked to specialized populations of pacemaker cells expressing vimentin, c-kit and Ca²⁺-activated-Cl^– channels, like interstitial cells of Cajal (ICC) in the gastrointestinal (GI) tract. While contractions of urethral muscles do not manifest as coordinated phasic contractions, in these species ICC-like cells might pace individual USMC bundles (through activation of voltage-gated Ca²⁺ channels) to contract asynchronously, with contractions of multiple bundles summating as tone. In mice, USMC are indeed rhythmically active (firing propagating Ca²⁺ waves linked to contraction), and this rhythmicity is asynchronous across the tissue, summating to form tone. However, experiments in mice have failed to demonstrate a voltage-dependent mechanism for regulating this rhythmicity or contractions in situ, suggesting that urethral tone results from intrinsic abilities of USMC to ‘pace’ their own Ca²⁺ mobilization to generate Ca²⁺ waves required for contraction. During the filling phase, animal and human bladders exhibit small transient increases in intravesical pressure, brought about by locally propagating transient contractions of the bladder wall. These transient contractions are critical in regulating sensory afferent activity – relaying sensations of bladder fullness to the CNS. Ex-vivo DSM strips exhibit spontaneous rhythmic contractions, mimicking transient concentrations observed during filling in-vivo. While DSM spontaneous contractions appear to an intrinsic myogenic property, they are regulated by autonomic nerves and urothelium.  Action potentials and associated rises in DSM cytosolic Ca²⁺ are essential for generating these contractions, with this activity appearing to be voltage dependent. The presence of putative ‘pacemaker’ interstitial cells in the DSM layers have been controversial. Similar, to the GI tract and urethra, Kit⁺ cells are present in the DSM layer, however, unlike these other organs these Kit⁺ cells are almost exclusively mast cells and thus unlikely to serve as pacemakers. However, another interstitial cell with immunopositivity for antibodies against PDGFRα, has recently been suggested to regulate DSM excitability by potentially serving as mechano and neural transducers, through activation of inhibitory purinergic-SK3 pathways. While the mechanics of rhythmic or tonic contractions in both bladder and urethra is myogenic, there are clear disparities in the cell types, molecular pathways and mechanisms of coordination that lead to these physiological behaviours in both organs.