Overactive bladder (OAB) has been increasingly associated with autonomic dysregulation. However, direct in vivo assessment of sympathetic drive remains technically challenging. This study aimed to determine whether skin sympathetic nerve activity (SKNA), recorded non-invasively from body surface sites, accurately reflects underlying sympathetic hyperactivity in a rat model of OAB induced by partial bladder outlet obstruction (pBOO).

Eight female Sprague–Dawley rats were included (Sham, n = 4; pBOO, n = 4). pBOO was induced via partial urethral ligation, while Sham animals underwent urethral exposure only. Sympathetic activity was simultaneously recorded from thoracic skin, abdominal skin, and directly from the sympathetic ganglion within a Faraday cage. Mean signal amplitude (µV) was quantified at each site. Between-group differences were analyzed using one-tailed Welch’s t-tests (pBOO > Sham), with effect sizes calculated as Cohen’s d. A composite sympathetic index was generated by averaging z-scores across the three recording sites. Fisher’s method was applied to integrate site-specific p-values.

Compared with Sham controls, pBOO rats exhibited characteristic OAB features, including increased voiding frequency, reduced voided volume, and increased bladder weight (all p < 0.05) (Fig. A). Sympathetic nerve activity was consistently elevated in the pBOO group across thoracic skin, abdominal skin, and direct ganglionic recordings (Fig. B). Fisher’s combined analysis confirmed overall sympathetic overactivation (p = 0.045). The composite three-site index demonstrated significantly increased sympathetic activity in pBOO rats (p = 0.013) (Fig. C). Notably, even when limited to the two skin recording sites, the non-invasive composite index remained significantly elevated (p = 0.027) (Fig. D), supporting the reliability of skin-derived measurements as a surrogate for sympathetic drive.

The present findings demonstrate a consistent and robust increase in sympathetic nerve activity in the pBOO-induced OAB model across both direct ganglionic and skin-based recordings. The strong concordance between invasive and non-invasive measurements supports the physiological validity of SKNA as a surrogate of systemic sympathetic drive. Importantly, the persistence of significant differences when analysis was restricted to skin recordings alone highlights the reliability and translational potential of SKNA as a non-invasive tool for assessing autonomic dysfunction in OAB.

Skin sympathetic nerve activity provides a reliable and non-invasive biomarker of sympathetic overactivation in overactive bladder. These findings establish a critical translational foundation for incorporating surface SKNA into clinical evaluation and monitoring of autonomic dysfunction in OAB.