Podium Session

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PD01-04: Stress induced visceral pain is mediated by alpha 1A adrenoceptors

Friday, May 12
7:30 AM - 7:40 AM
Location: BCEC: Room 159

Presentation Authors: Rita Matos, Paula Serrão, Porto, Portugal, Larissa Rodriguez, Los Angeles, CA, Lori Birder, Pittsburgh, PA, Francisco Cruz*, Ana Charrua, Porto, Portugal

Introduction: Chronic water avoidance stress (WAS) result in long-standing bladder pain and exhibits many of the findings observed in BPS/IC patients. However, the exact mechanism by which WAS induces visceral pain is unknown.
Since chronic stimulation of alpha1A adrenoceptors increases the activity of bladder nociceptors, we investigate if changes induced by WAS are mediated by a similar adrenergic mechanism.


Methods: WAS was induced in adult female Wistar rats by placing the animals on a pedestal in the centre of a cage filled with water at room temperature, for 1h/day, for 10 consecutive days. Lower abdomen pain threshold was measured using von Frey filaments, at baseline (day 0) and after WAS (day 11). Colonic activity was also measured at day 0 and day 11. At day 12, WAS were anaesthetised, urine collected and noradrenaline levels by determined HPLC, and bladder frequency determined by cystometry. Bladders were harvested, sectioned and stained with HE to analyse urothelium integrity and with Toluidine blue to quantify mast cells. These experiments were repeated in WAS animals treated with the alpha1A AR Silodosin (0.2 mg/kg.day). Non-stressed rats were used as controls. Comparisons were done using T-test and Kruskal-Wallis followed from Dunn's Multiple Comparisons Test.

Results: The results are summarized in table 1.



Conclusions: WAS result in an increase in noradrenaline urinary levels, suggesting the involvement of the adrenergic system. As silodosin treatment prevented the development of bladder pain, bladder hyperactivity and mast cells accumulation, alpha 1A AR is likely to play a role in chronic adrenergic stimulation associated with WAS. These findings may be relevant for the treatment of BPS/IC.

Source Of Funding: Ana Charrua is supported by Fundacao para a Ciencia e Tecnologia (FCT) fellowship SFRH/BPD/68716/2010.
This work was supported by the PFD Research Foundation and ICA IC/PBS Research Grant.

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