Modulation of Stretch Evoked Adenosine Triphosphate Release From Bladder Epithelium by Prostaglandin E
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Tanaka, Ippei; Nagase, Keiko; Tanase, Kazuya; Aoki, Yoshitaka; Akino, Hironobu; Yokoyama, Osamu

doi:10.1016/j.juro.2010.09.042

Cited by 30 publications

(22 citation statements)

References 24 publications

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“…Furthermore, in another study in rat bladders studied in an organ bath model it was shown that PGE 2 release could be antagonized by indomethacin and concluded that COX inhibitors suppress ATP release from bladder epithelium via decreasing PGE 2 . In addition, EP1 and/or EP3 receptors were suggested to participate in this effect [24]. In a study in rabbit detrusor strips it was shown that both indomethacin and ibuprofen suppress spontaneous contractions [25].…”

Section: Discussionmentioning

confidence: 99%

The effect of indomethacin on the muscarinic induced contractions in the isolated normal guinea pig urinary bladder

et al. 2013

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BackgroundTo investigate the effect of prostaglandin depletion by means of COX-inhibition on cholinergic enhanced spontaneous contractions.MethodsThe urethra and bladder of 9 male guinea pigs (weight 270–300 g) were removed and placed in an organ bath with Krebs’ solution. A catheter was passed through the urethra through which the intravesical pressure was measured. The muscarinic agonist arecaidine, the non-selective COX inhibitor indomethacin, and PGE2 were subsequently added to the organ bath. The initial average frequency and amplitude of spontaneous contractions in the first 2 minutes after arecaidine application were labelled Fini and Pini, respectively. The steady state frequency (Fsteady) and amplitude (Psteady) were defined as the average frequency and amplitude during the 5 minutes before the next wash out.ResultsApplication of 1 μM PGE2 increased the amplitude of spontaneous contractions without affecting frequency. 10 μM of indomethacin reduced amplitude but not frequency.The addition of indomethacin did not alter Fini after the first application (p = 0.7665). However, after the second wash, Fini was decreased (p = 0.0005). Fsteady, Psteady and Pini were not significantly different in any of the conditions. These effects of indomethacin were reversible by PGE2 addition..ConclusionsBlocking PG synthesis decreased the cholinergically stimulated autonomous contractions in the isolated bladder. This suggests that PG could modify normal cholinergically evoked response. A combination of drugs inhibiting muscarinic receptors and PG function or production can then become an interesting focus of research on a treatment for overactive bladder syndrome.

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Section: Discussionmentioning

confidence: 99%

The effect of indomethacin on the muscarinic induced contractions in the isolated normal guinea pig urinary bladder

et al. 2013

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“…Cyclooxygenase inhibitors suppress ATP release from rat bladder epithelium via decreasing PGE 2 action via prostanoid EP1 and/or EP3 receptors [660]. Both the vanilloid and acid-sensing ion channel (ASIC) systems contribute to acidinduced ATP release from urothelial cells [586].…”

Section: Ectoenzymatic Breakdown Of Atpmentioning

confidence: 99%

Purinergic signalling in the urinary tract in health and disease

Burnstock

2013

Purinergic Signalling

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Purinergic signalling is involved in a number of physiological and pathophysiological activities in the lower urinary tract. In the bladder of laboratory animals there is parasympathetic excitatory cotransmission with the purinergic and cholinergic components being approximately equal, acting via P2X1 and muscarinic receptors, respectively. Purinergic mechanosensory transduction occurs where ATP, released from urothelial cells during distension of bladder and ureter, acts on P2X3 and P2X2/3 receptors on suburothelial sensory nerves to initiate the voiding reflex, via low threshold fibres, and nociception, via high threshold fibres. In human bladder t h e p u r i n e rg i c c o m p o n e n t o f p a r a s y m p a t h e t i c cotransmission is less than 3 %, but in pathological conditions, such as interstitial cystitis, obstructed and neuropathic bladder, the purinergic component is increased to 40 %. Other pathological conditions of the bladder have been shown to involve purinoceptor-mediated activities, including multiple sclerosis, ischaemia, diabetes, cancer and bacterial infections. In the ureter, P2X7 receptors have been implicated in inflammation and fibrosis. Purinergic therapeutic strategies are being explored that hopefully will be developed and bring benefit and relief to many patients with urinary tract disorders.

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“…Prostanoid production in the bladder wall is well established, with prostanoids known to be synthesized locally within both the mucosa and smooth muscle and they are thought to play a role in the sensory arm of the micturition reflex. Urothelial production of prostanoids has been demonstrated in the bladder of most species including rat (Pinna et al, 1992, Tanaka et al, 2011, rabbit (Masick et al, 2001, Azadzoi et al, 2004, guinea pig (Saban et al, 1994, Nile et al, 2010, Guan et al, 2014 and human (Jeremy et al, 1987). Cyclooxygenase 1 is markedly localized to the urothelium and expressed within the basal and intermediate cells (de Jongh et al, 2009), although not in the umbrella cells (Rahnama'i et al, 2012).…”

Section: Prostaglandinsmentioning

confidence: 99%

Modulation of lower urinary tract smooth muscle contraction and relaxation by the urothelium

Sellers

Chess-Williams

Michel

2018

Naunyn-Schmiedeberg's Arch Pharmacol

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The epithelial inner layer of the lower urinary tract, i.e., the urothelium, and other parts of the mucosa are not just a passive barrier but play an active role in the sensing of stretching, neurotransmitters, paracrine mediators, hormones, and growth factors and of changes in the extracellular environment. We review the molecular and cellular mechanisms enabling the urothelium to sense such inputs and how this leads to modulation of smooth muscle contraction and relaxation. The urothelium releases various mediators including ATP, acetylcholine, prostaglandins, nitric oxide, and nerve growth factor. These may affect function and growth of smooth muscle cells and afferent nerves. However, the molecular identity of the urothelium-derived mediator directly modulating contractile and relaxant responses of isolated bladder strips has remained elusive. The morphology and function of the urothelium undergo changes with aging and in many pathophysiological conditions. Therefore, the urothelium may contribute to the therapeutic effects of established drugs to treat lower urinary tract dysfunction and may also serve as a target for novel therapeutics. However, therapeutics may also change urothelial function, and it is not always easy to determine whether such changes are part of the therapeutic response or reflect secondary alterations.

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Modulation of Stretch Evoked Adenosine Triphosphate Release From Bladder Epithelium by Prostaglandin E ₂

Abstract: Results indicate that cyclooxygenase inhibitors suppress adenosine triphosphate release from bladder epithelium via decreasing prostaglandin E(2). EP1 and/or EP3 receptors appear to participate in this effect.

Cited by 30 publications

References 24 publications

The effect of indomethacin on the muscarinic induced contractions in the isolated normal guinea pig urinary bladder

The effect of indomethacin on the muscarinic induced contractions in the isolated normal guinea pig urinary bladder

Purinergic signalling in the urinary tract in health and disease

Modulation of lower urinary tract smooth muscle contraction and relaxation by the urothelium

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Modulation of Stretch Evoked Adenosine Triphosphate Release From Bladder Epithelium by Prostaglandin E 2

Abstract: Results indicate that cyclooxygenase inhibitors suppress adenosine triphosphate release from bladder epithelium via decreasing prostaglandin E(2). EP1 and/or EP3 receptors appear to participate in this effect.

Cited by 30 publications

References 24 publications

The effect of indomethacin on the muscarinic induced contractions in the isolated normal guinea pig urinary bladder

The effect of indomethacin on the muscarinic induced contractions in the isolated normal guinea pig urinary bladder

Purinergic signalling in the urinary tract in health and disease

Modulation of lower urinary tract smooth muscle contraction and relaxation by the urothelium

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Modulation of Stretch Evoked Adenosine Triphosphate Release From Bladder Epithelium by Prostaglandin E ₂