Receptor GPR91 contributes to voiding function and detrusor relaxation mediated by succinate
Abubakr Mossa, Monica Velasquez-Flores1, Philippe G Cammisotto1
1Lady Davis Institute, McGill University, Montreal, Quebec, Canada.
Neurourology and Urodynamics
|October 24, 2020
Summary
Succinate activates the GPR91 receptor in the bladder, impacting bladder structure and function. GPR91 mediates bladder relaxation by reducing urothelial ATP secretion.
Area of Science:
- Urology
- Physiology
- Biochemistry
Background:
- Succinate is known to activate the GPR91 receptor.
- GPR91 has been identified in the bladder, suggesting a role in its function.
Purpose of the Study:
- To investigate the mechanisms by which succinate induces bladder relaxation.
- To determine the role of the GPR91 receptor in succinate-mediated bladder changes.
Main Methods:
- Cystometry and organ bath studies were performed on wild-type and GPR91 knockout mice, as well as Sprague-Dawley rats.
- GPR91 expression, tissue morphology, nitric oxide (NO), and ATP secretion were analyzed.
Main Results:
- GPR91 knockout mice exhibited altered bladder structure and impaired bladder function, including increased wall thickness and pressure.
- Succinate induced bladder relaxation in wild-type but not GPR91 knockout mice, indicating GPR91 dependence.
- Succinate decreased urothelial ATP secretion in a GPR91-dependent manner, contributing to detrusor relaxation.
Conclusions:
- GPR91 is crucial for maintaining normal bladder structure and contraction.
- GPR91-mediated bladder relaxation is partially achieved by reducing urothelial ATP secretion.
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