TRPV1 alterations in urinary bladder dysfunction in a rat model of STZ-induced diabetes

Sharopov, Bizhan R.; Gulak, Kseniya L.; Philyppov, Igor B.; Sotkis, A. V.; Shuba, Yaroslav

doi:10.1016/j.lfs.2017.10.042

Cited by 18 publications

(14 citation statements)

References 38 publications

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“…4c,d), although for EFS-contractions the difference did not rich statistical significance. In view of the fact that TRPV1 activation in isolated bladder preparations is thought to produce contractions through the release of tachykinins from CAP-sensitive TRPV1-expressing bladder afferents 25,28 , these findings suggest upregulation of TRPV1 expression, stronger TRPV1 coupling with tachykinin release machinery and/or enhancement of tachykinin-mediated DSM contractility in bladder cancer. Such alterations would favour both strengthening of TRPV1-dependent afferent limb of micturition reflex and potentiation of local TRPV1-dependent "efferent" functions of bladder afferents, consistent with the promotion of urge incontinence.…”

Section: Efs-evoked Contractions Electric Field Stimulation (Efs) Ofmentioning

confidence: 92%

“…Whether or not it is also present on functionallyrelevant levels in other bladder tissues, first of all in the urothelium, still remains the matter of controversy 27 . On the local level, TRPV1 activation in CAP-sensitive, TRPV1-expressing bladder afferents may induce DSM contraction via their "efferent" functions through the release of tachykinins, neuropeptides with contractile action on DSM 25,28 . Thus, while TRPV1 sensory function is responsible for the perception of pain and afferent limb of micturition reflex, its "efferent" activity is involved in the local control of nerve excitability and smooth muscle contractility.…”

Section: Efs-evoked Contractions Electric Field Stimulation (Efs) Ofmentioning

confidence: 99%

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Alterations in detrusor contractility in rat model of bladder cancer

Philyppov

Sotkis

Röck

et al. 2020

Sci Rep

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Urinary incontinence of idiopathic nature is a common complication of bladder cancer, yet, the mechanisms underlying changes in bladder contractility associated with cancer are not known. Here by using tensiometry on detrusor smooth muscle (DSM) strips from normal rats and rats with bladder cancer induced by known urothelial carcinogen, N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), we show that bladder cancer is associated with considerable changes in DSM contractility. These changes include: (1) decrease in the amplitude and frequency of spontaneous contractions, consistent with the decline of luminal pressures during filling, and detrusor underactivity; (2) diminution of parasympathetic DSM stimulation mainly at the expense of m-cholinergic excitatory transmission, suggestive of difficulty in bladder emptying and weakening of urine stream; (3) strengthening of TRPV1-dependent afferent limb of micturition reflex and TRPV1-mediated local contractility, promoting urge incontinence; (4) attenuation of stretch-dependent, TRPV4-mediated spontaneous contractility leading to overflow incontinence. These changes are consistent with the symptomatic of bladder dysfunction in bladder cancer patients. Considering that BBN-induced urothelial lesions in rodents largely resemble human urothelial lesions at least in their morphology, our studies establish for the first time underlying reasons for bladder dysfunction in bladder cancer.

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Section: Efs-evoked Contractions Electric Field Stimulation (Efs) Ofmentioning

confidence: 92%

Section: Efs-evoked Contractions Electric Field Stimulation (Efs) Ofmentioning

confidence: 99%

Alterations in detrusor contractility in rat model of bladder cancer

Philyppov

Sotkis

Röck

et al. 2020

Sci Rep

Self Cite

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“…Intravesical capsaicin has been shown to ameliorate symptoms of detrusor hyperreflexia and is in clinical use to treat this condition [107]. A decrease in TRPV1 receptor agonist-induced urinary bladder contraction has been shown in streptozotocin-induced experimental diabetes [108]. This may be explained by a loss of sensory nerves, impaired axonal transport or expression of the TRPV1 receptor [108].…”

Section: Contribution Of Trpv1 Receptor-and Insr-expressing Psns To Pmentioning

confidence: 99%

“…A decrease in TRPV1 receptor agonist-induced urinary bladder contraction has been shown in streptozotocin-induced experimental diabetes [108]. This may be explained by a loss of sensory nerves, impaired axonal transport or expression of the TRPV1 receptor [108]. Importantly, changes in TRPV1 receptor gene expression may also contribute to a decrease of TRPV1 receptor agonist-induced smooth muscle contraction since, in neuroblastoma cells, TRPV1 receptor gene transcription has been shown to be insulin-dependent [21].…”

Section: Contribution Of Trpv1 Receptor-and Insr-expressing Psns To Pmentioning

confidence: 99%

Modulation of Sensory Nerve Function by Insulin: Possible Relevance to Pain, Inflammation and Axon Growth

Lázár

Jancsó

Stella

2020

IJMS

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Insulin, besides its pivotal role in energy metabolism, may also modulate neuronal processes through acting on insulin receptors (InsRs) expressed by neurons of both the central and the peripheral nervous system. Recently, the distribution and functional significance of InsRs localized on a subset of multifunctional primary sensory neurons (PSNs) have been revealed. Systematic investigations into the cellular electrophysiology, neurochemistry and morphological traits of InsR-expressing PSNs indicated complex functional interactions among specific ion channels, proteins and neuropeptides localized in these neurons. Quantitative immunohistochemical studies have revealed disparate localization of the InsRs in somatic and visceral PSNs with a dominance of InsR-positive neurons innervating visceral organs. These findings suggested that visceral spinal PSNs involved in nociceptive and inflammatory processes are more prone to the modulatory effects of insulin than somatic PSNs. Co-localization of the InsR and transient receptor potential vanilloid 1 (TRPV1) receptor with vasoactive neuropeptides calcitonin gene-related peptide and substance P bears of crucial importance in the pathogenesis of inflammatory pathologies affecting visceral organs, such as the pancreas and the urinary bladder. Recent studies have also revealed significant novel aspects of the neurotrophic propensities of insulin with respect to axonal growth, development and regeneration.

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“…Here, TRPV1 mediates, at least in part, mechanosensation of the bladder during its filling, but little is known if these channels could interact with purinergic P2X receptors modulating ATP release from the urothelium and ATP-sensitivity of the afferent fibers [115]. TRPV1 expression appears to be altered in diabetic bladder dysfunction [116]. Capsaicin and resiniferatoxin, which cause desensitization of TRPV1, were used to treat neurogenic detrusor overactivity, but together with channel antagonists like GRC-6211 that reduces bladder contraction frequency, these demonstrated significant side effects [117].…”

Section: Trpv1 In Vascular and Visceral Systemsmentioning

confidence: 99%

Multifunctional TRPV1 Ion Channels in Physiology and Pathology with Focus on the Brain, Vasculature, and Some Visceral Systems

Storozhuk

Moroz

Zholos

2019

BioMed Research International

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TRPV1 has been originally cloned as the heat and capsaicin receptor implicated in acute pain signalling, while further research has shifted the focus to its importance in chronic pain caused by inflammation and associated with this TRPV1 sensitization. However, accumulating evidence suggests that, apart from pain signalling, TRPV1 subserves many other unrelated to nociception functions in the nervous system. In the brain, TRPV1 can modulate synaptic transmission via both pre- and postsynaptic mechanisms and there is a functional crosstalk between GABA receptors and TRPV1. Other fundamental processes include TRPV1 role in plasticity, microglia-to-neuron communication, and brain development. Moreover, TRPV1 is widely expressed in the peripheral tissues, including the vasculature, gastrointestinal tract, urinary bladder, epithelial cells, and the cells of the immune system. TRPV1 can be activated by a large array of physical (heat, mechanical stimuli) and chemical factors (e.g., protons, capsaicin, resiniferatoxin, and endogenous ligands, such as endovanilloids). This causes two general cell effects, membrane depolarization and calcium influx, thus triggering depending on the cell-type diverse functional responses ranging from neuronal excitation to secretion and smooth muscle contraction. Here, we review recent research on the diverse TRPV1 functions with focus on the brain, vasculature, and some visceral systems as the basis of our better understanding of TRPV1 role in different human disorders.

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TRPV1 alterations in urinary bladder dysfunction in a rat model of STZ-induced diabetes

Cited by 18 publications

References 38 publications

Alterations in detrusor contractility in rat model of bladder cancer

Alterations in detrusor contractility in rat model of bladder cancer

Modulation of Sensory Nerve Function by Insulin: Possible Relevance to Pain, Inflammation and Axon Growth

Multifunctional TRPV1 Ion Channels in Physiology and Pathology with Focus on the Brain, Vasculature, and Some Visceral Systems

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