813 Increased Sympathetic Activity Enhances Bladder Hyperactivity and Triggers Bladder Pain

Charrua, Ana; Rodrigues-Pinto, Ricardo; Taylor, Anne L.; Barros, Sérgio; Ribeiro‐da‐Silva, Alfredo; Cruz, Carlos Oliveira; Avelino, António; Cruz, Francisco

doi:10.1016/j.juro.2011.02.631

Cited by 3 publications

(3 citation statements)

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“…The downstream effectors of these pathways, including CRF, cortisol, and noradrenaline are well known regulators of urinary function and thought to be crucial in regulating centrally mediated changes that induce IC/BPS symptoms (Ulrich- Lai and Herman, 2009;Pierce and Christianson, 2015). Furthermore, clinical studies have revealed that chronic psychological stress induces heightened inflammatory responses in peripheral tissues, including elevated levels of circulating proinflammatory cytokines, and mastocytosis in the bladder (Charrua et al, 2015). Crucially, stress alleviation has been shown to be effective in reducing the severity of IC/BPS symptoms in some patients (Bosch and Bosch, 2014;Webster and Brennan, 1998;Carrico et al).…”

Section: Chronic Stressmentioning

confidence: 99%

Animal models of interstitial cystitis/bladder pain syndrome

Tay,

Grundy

2023

Front. Physiol.

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Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS) is a chronic disorder characterized by pelvic and/or bladder pain, along with lower urinary tract symptoms that have a significant impact on an individual’s quality of life. The diverse range of symptoms and underlying causes in IC/BPS patients pose a significant challenge for effective disease management and the development of new and effective treatments. To facilitate the development of innovative therapies for IC/BPS, numerous preclinical animal models have been developed, each focusing on distinct pathophysiological components such as localized urothelial permeability or inflammation, psychological stress, autoimmunity, and central sensitization. However, since the precise etiopathophysiology of IC/BPS remains undefined, these animal models have primarily aimed to replicate the key clinical symptoms of bladder hypersensitivity and pain to enhance the translatability of potential therapeutics. Several animal models have now been characterized to mimic the major symptoms of IC/BPS, and significant progress has been made in refining these models to induce chronic symptomatology that more closely resembles the IC/BPS phenotype. Nevertheless, it's important to note that no single model can fully replicate all aspects of the human disease. When selecting an appropriate model for preclinical therapeutic evaluation, consideration must be given to the specific pathology believed to underlie the development of IC/BPS symptoms in a particular patient group, as well as the type and severity of the model, its duration, and the proposed intervention’s mechanism of action. Therefore, it is likely that different models will continue to be necessary for preclinical drug development, depending on the unique etiology of IC/BPS being investigated.

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Section: Chronic Stressmentioning

confidence: 99%

Animal models of interstitial cystitis/bladder pain syndrome

Tay,

Grundy

2023

Front. Physiol.

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“…There is a fast-growing body of publications showing the complex relationship between pain conditions and activity of ANS centres [25]. There are many examples of this co-existence in people with diseases of various systems: cardiovascular [26]; respiratory [27,28]; digestive [29,30]; genitourinary [31,32]; immune [33]; thermoregulation [34]; cerebral circulation and headaches [35][36][37]; sleep and circadian rhythms [38,39]. Many of the above publications and similar are observational studies (and rarely prospective) or reviews.…”

Section: Central Ansmentioning

confidence: 99%

The Role of Autonomic Nervous System in Pain Chronicity

Kruglov¹,

McGuckin²

2023

Topics in Autonomic Nervous System

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The role of the autonomic nervous system (ANS) in chronic pain (CP) and in its chronicity is considered secondary and reactive to the nociceptive processes in the somatic nervous system (SomNS). However, research and clinical data strongly suggest the opposite. The ANS is an ancient, complex and ample part of the nervous system. It serves and controls visceral organs and somatic tissues. The ANS takes part in all aspects of all types of pain and influences its mechanisms at both peripheral and central levels. In this chapter we bring together the evidence from biomedical disciplines and clinical practice to support an alternative theory which contradicts the traditional views on the subject. We also raise questions which require further research to consolidate facts, advance our knowledge and improve treatment strategies for CP. The importance of this topic is difficult to overestimate because of the significant impact of CP on society and the lack of understanding, efficient therapy or cure.

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“…The sympathetic nervous system, traditionally identified in fight-orflight response, is increasingly recognized for its role in modulation of pain. 8,21,39 In response to inflammation or nerve injury, the unmyelinated postganglionic sympathetic nerve fibers that use norepinephrine (NE) as their neurotransmitters pass the gray rami communicans to sprout into dorsal root ganglia (DRG). 35,60 A localized sympathectomy that cuts the sympathetic postganglionic axons in the gray rami reduces mechanical hypersensitivity in neuropathic pain.…”

Section: Introductionmentioning

confidence: 99%

Beta 2-adrenergic receptor mediates noradrenergic action to induce cyclic adenosine monophosphate response element-binding protein phosphorylation in satellite glial cells of dorsal root ganglia to regulate visceral hypersensitivity

Shen

Tiwari

Madar

et al. 2021

Pain

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Sympathoneuronal outflow into dorsal root ganglia (DRG) is suggested to be involved in sympathetically maintained chronic pain, which is mediated by norepinephrine (NE) action on DRG cells. This study combined in vitro and in vivo approaches to identify the cell types of DRG that received NE action and examined cell type-specific expression of adrenergic receptors (ARs) in DRG. Using DRG explants, we identified that NE acted on satellite glial cells (SGCs) to induce the phosphorylation of cAMP response element-binding protein (CREB). Using primarily cultured SGCs, we identified that beta (b)2-adrenergic receptor but not alpha (a)adrenergic receptor nor other bAR isoforms mediated NE-induced CREB phosphorylation and CRE-promoted luciferase transcriptional activity. Using fluorescence in situ hybridization and affinity purification of mRNA from specific cell types, we identified that b2AR was expressed by SGCs but not DRG neurons. We further examined b2AR expression and CREB phosphorylation in vivo in a model of colitis in which sympathetic nerve sprouting in DRG was observed. We found that b2AR expression and CREB phosphorylation were increased in SGCs of thoracolumbar DRG on day 7 after colitis induction. Inhibition but not augmentation of b2AR reduced colitis-induced calcitonin generelated peptide release into the spinal cord dorsal horn and colonic pain responses to colorectal distention. Prolonged activation of b2AR in naive DRG increased calcitonin gene-related peptide expression in DRG neurons. These findings provide molecular basis of sympathetic modulation of sensory activity and chronic pain that involves b2AR-mediated signaling in SGCs of DRG.

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813 Increased Sympathetic Activity Enhances Bladder Hyperactivity and Triggers Bladder Pain

Cited by 3 publications

References 0 publications

Animal models of interstitial cystitis/bladder pain syndrome

Animal models of interstitial cystitis/bladder pain syndrome

The Role of Autonomic Nervous System in Pain Chronicity

Beta 2-adrenergic receptor mediates noradrenergic action to induce cyclic adenosine monophosphate response element-binding protein phosphorylation in satellite glial cells of dorsal root ganglia to regulate visceral hypersensitivity

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