Abstract
AIMS: The aim of this study is to elucidate the pathophysiological mechanisms of urethral instability by analyzing and comparing cystometric data from a female individual with urethral instability and another with normal micturition. METHODS: Data were collected from a previous study measuring urethral pressure at three distinct points within the urethra, along with continuous needle electromyography (EMG) recordings of the external striated urethral sphincter. A comprehensive literature review on the function of different urethral muscle groups was also conducted to support the findings. RESULTS: The findings suggest that urethral instability primarily results from a loss of smooth muscle closure function. This condition is triggered by the interaction of pre-existing high urethral tension and low-level vesical afferent firing at the onset of bladder filling, causing relaxation of the urethral smooth musculature and impaired closure function of the urethra. The subsequent entry of fluid into the proximal urethra induces reflex contractions of the external sphincter, in an attempt to close the urethra and prevent urine loss and manifests as urethral instability. Compared to normal micturition, which shows a gradual decline in urethral pressure, the subject with instability exhibited rapid fluctuations in urethral pressure and EMG activity. CONCLUSIONS: This study highlights the role of smooth urethral musculature in maintaining urethral closure function during bladder filling. Therapeutic approaches should focus on reducing basal urethral tension to preserve smooth muscle closure function during bladder filling. Future research may explore pharmacological interventions, particularly adrenergic beta-3 receptor agonists or alpha blockers, as potential treatments for urethral instability.