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Introduction: Using immunohistochemistry and RT-PCR, we previously documented the presence of TRPV3 in the urinary bladder and its sensory pathways as well as its upregulation in a mouse model of detrusor overactivity. A combination of TRPA1 and TRPV3 antagonists decreases detrusor muscle tone in vitro to a greater degree than either one alone. The goal of this study was to further evaluate the functional role of TRPV3 and to test if the naturally occurring TRPA1 and V3 modulator carvacrol can suppress detrusor hyperactivity.
Materials & Methods: Overnight 12-hour micturition frequency were compared between wild type (WT, n=12) and TRPV3-knockout (n=14) mice based on the number of urine spots detected on filter paper placed beneath the cage. Using cystometry and multifiber sensory recording, changes in bladder function and its nerve activity were studied in a conscious animal model of acetic acid-induced bladder hyperactivity before and after administration of carvacrol (n=5).
Results: Compared to WT animals, the voiding frequency in TRPV3-knockout animals was 59% longer. In the same group of animals, cystometry recordings showed a significant increase in the inter-micturition interval. Intravesical infusion of 0.25% acetic acid caused a reduction in functional bladder capacity. Adding carvacrol to the intravesical infusion containing acetic acid returned functional bladder capacity and sensory nerve activity to normal.
Conclusions: This study provides further evidence that the TRPV3 channel has a functional role in the urinary bladder and that potential therapeutic effect could be increased by synergistically targeting both TRPA1 and TRPV3 ion channels.