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• W313811541 abstract "Bladder painful syndrome/ interstitial cystitis (BPS/IC) is a chronic debilitating condition with unknown etiology. Patients with BPS/IC present an increased sympathetic activity, characterized by an increase in tyrosine hydroxylase expression in the bladder, increased noradrenaline levels in urine and elevated mean blood pressure and heart rate during bladder hydrodistention. These patients also present an increase in expression of TRPV1 in the bladder. Sympathetic overactivity also can be observed in several human painful diseases and in rat pain models. Previous studies showed that chronic adrenergic stimulation with phenylephrine (PHE) in rats induced pain behavior, increased voiding frequency and urothelial dysfunction, which mimic BPS/IC. Pain and increased frequency where dependent of capsaicin sensitive primary afferents activation since desensitization of these fibers with high levels of capsaicin reverse the phenylephrine mediated effect, demonstrating a possible relation between adrenergic activity and nociceptive activity (like TRPV1 or other receptors like cannabinoid receptors, for example). Hence, this work had three main goals. The first goal was to demonstrate the involvement of adrenoceptors in the appearance of BPS/IC symptoms, characterizing which subtypes are involved in the appearance of pain and histological changes observed in animals submitted to chronic adrenergic stimulation with phenylephrine. The second aim was to evaluate the cross-talk between adrenoceptors and TRPV1 during chronic adrenergic stimulation with phenylephrine. The third aim was to verify how endocannabinoids modulate the bladder pain and hyperactivity during cystitis. To assess which adrenoceptor subtypes are involved in the appearance of pain, to female Wistar rats injected with 2.5 mg/Kg/day of phenylephrine (PHE; subcutaneously for 14 days) was administrated orally the follow antagonists of adrenoceptors: Silodosin, Naftopidil or Prazosin. The visceral pain behavior and voiding pattern were analyzed before and 14 days after PHE treatment. At day 15, animals were anaesthetized with urethane (1.2 g/Kg) and cystometries were performed for 2h. Animals were then perfused with paraformaldehyde and the bladder and L6 spinal cord segments were harvested. Bladder sections from these animals were stained with Hematoxylin-eosin to analyze urothelium morphology, with Toluidine Blue FCUP Characterization of an animal model of Bladder painful syndrome/ Interstitial cystitis 12 to study mast cells, and immunoreacted (IR) against caspase 3, to investigate urothelial apoptosis. L6 spinal cord segments were IR against Fos. Furthermore, to study the cross-talk between adrenoceptors and nociceptive pathways, a group of TRPV1 knockout mice were injected with PHE daily for 14 days. Visceral pain behavior and cystometry were performed in these animals. Further, a group of female Wistar rats was daily injected with phenylephrine for 14 days. At the end of treatment, animals were submitted to cystometry with capsaicin. To assess if endocannabinoids modulate bladder pain and hyperactivity during cystitis, a group of female Wistar rats were instilled with lipopolysaccharide (LPS) and URB (inhibitor of FAAH, fatty acid amide hydrolase). Visceral pain behavior and cystometry were performed. These experiments were repeated in rats co-treated with LPS, URB and antagonists of CB1, CB2 and TRPV1 (MJ15, SR144528 and SB366791, respectively). L6 spinal cord segments were IR against Fos. The results confirm that chronic adrenergic stimulation with PHE induce visceral pain, mast cells infiltration, apoptosis of urothelial cells and activation of nociceptive pathways. Silodosin (antagonist of α1A-adrenoceptor subtype) seem to be more effective than naftopidil or prazosin (α1D and α1-adrenoceptor antagonists, respectively) to reduce the effects induced by PHE. This work also shows that TRPV1 and CB1 are involved in bladder hyperactivity. Thus, it can be affirmed that BPS/IC result the interaction between several pathways, namely those involving α1A-adrenoceptors, TRPV1 and CB1." @default.
• W313811541 created "2016-06-24" @default.
• W313811541 creator A5014952281 @default.
• W313811541 date "2014-10-24" @default.
• W313811541 modified "2023-09-27" @default.
• W313811541 title "Characterization of an animal model of Bladder painful syndrome/interstitial cystitis" @default.
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