Comparison of the mode of action of prostaglandin E2 (PGE2) and sulprostone, a PGE2-derivative, on the lower urinary tract in healthy women

Schüßler, B.

doi:10.1007/bf00300786

Cited by 71 publications

(53 citation statements)

References 15 publications

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“…3 Intravesical administration of PGE2 stimulated reflex micturition in human and rats, while administration of EP1 receptor antagonist improved bladder storage function in rats. [4][5][6] These studies indicated the involvement of PGE2 via EP1 receptor in urinary frequency. There is a report that intravenous administration of EP1 antagonist relieved bladder pain in cystitis model rats.…”

Section: Textmentioning

confidence: 84%

Evaluation of Prostaglandin E2 and E-Series Prostaglandin Receptor in Patients with Interstitial Cystitis

et al. 2015

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Runninghead: Involvement of prostaglandin E2 in interstitial cystitisKey words: bladder pain syndrome, interstitial cystitis, prostaglandin E2 ABSTRACT (250 words)Purpose: To examine the precise role of prostaglandin E2 (PGE2) and E-series prostaglandin (EP) receptor in the pathophysiology of interstitial cystitis/bladder pain syndrome (IC/BPS). Materials and Methods:Twenty female patients with IC/BPS (11 ulcer-type and 9 non ulcer-type), 9 female controls with other urological diseases who needed cystoscopic procedure, and 10 normal female volunteers were enrolled. O'Leary-Sant Score (OSS) for symptoms and problems and voluntary urine for PGE2 analysis were obtained from all objectives. Under anesthesia, the bladder was distended by saline in a stepwise fashion (from 100 ml to maximum capacity) in patients with IC/BPS, and the infused saline was retrieved each time for PGE2 analysis. We also measured PGE2 and expression of EP receptors mRNA in bladder biopsy tissue in patients with IC/BPS.Results: Symptoms and problems index in patients with ulcer-type was significantly higher than those with non ulcer-type. Urinary PGE2 in patients with ulcer-type was significantly higher than those with non ulcer-type and normal volunteers. PGE2 level in retrieved saline in patients with ulcer-type increased depending on infusion volume, but not in those with non ulcer-type. PGE2 content in bladder biopsy tissue was significantly higher in patients with ulcer-type than controls. In patients with ulcer-type, expression of EP1 and EP2 mRNA was significantly higher than controls. Conclusions:Overproduction of PGE2 in the bladder seems to play a pathophysiological role in patients with ulcer-type IC/BPS via EP1 and EP2 receptors. Localized blockade of the action of PGE2 may lead to relieving symptoms in patients with ulcer-type IC/BPS. TEXTInterstitial cystitis/bladder pain syndrome (IC/BPS), non-specific inflammatory disease of the bladder, presents with a constellation of symptoms including urinary frequency, urgency and bladder pain. IC/BPS has 2 distinct subtypes based on cystoscopic evaluation. One is ulcer-type and another is non ulcer-type. In patients with IC/BPS and controls, samples were taken by cystoscopic procedure under general or spinal anesthesia. In patients with IC/BPS, the bladder was distended in a stepwise fashion with a drip infusion of saline. Saline bottles were placed at 80cm height from the symphysis pubis. First, cystoscope was inserted and the bladder was emptied. Then 100ml of saline was infused into the bladder as first step and maintained for 5 minutes. All of the infused saline was retrieved and sampled. Next, 200ml of saline was infused, maintained for 5 minutes, retrieved and sampled as second step. Third step and final step were similarly performed after 300ml saline infusion and maximum bladder capacity. Maximum bladder capacity was defined as bladder capacity at the time when saline infusion stopped after reaching 80cmH2O. In control patients, infused saline only at first step (100ml infusi...

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Section: Textmentioning

confidence: 84%

Evaluation of Prostaglandin E2 and E-Series Prostaglandin Receptor in Patients with Interstitial Cystitis

et al. 2015

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“…A more important physiologic role might be sensitization of afferent nerves. PGE2 instillation into the bladder produces DO, both in humans 81 and animals. 82 Evidence for an involvement of different prostanoid receptors (EP1, EP3, IP) in afferent signaling has been presented, 83 -86 making these receptors interesting drug targets.…”

Section: Local Mediators Influencing Spontaneous Activitymentioning

confidence: 99%

Detrusor myocyte activity and afferent signaling

Andersson

2009

Neurourology and Urodynamics

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Aims: To discuss (1) mechanisms involved in the generation and control of myocyte contractions and consequent afferent nerve activity and (2) these mechanisms as targets for drugs aimed for treatment of overactive bladder (OAB) symptoms and detrusor overactivity (DO). Methods: Literature review of myocyte activation, bladder afferent nerves, mediators in the bladder, and translational aspects of the findings. Results: During bladder filling, there is normally no parasympathetic outflow from the spinal cord. Despite this, the bladder develops tone during filling and also exhibits non-synchronized local contractions and relaxations that are caused by a basal myogenic mechanical activity that may be reinforced by release of, for example, acetylcholine from non-neuronal and/or neuronal sources or local mediators, such as prostaglandins and endothelins. It is suggested that these spontaneous contractions are able to generate activity in afferent nerves (''afferent noise'') that may contribute to DO and OAB. Conclusions: Spontaneous bladder myocyte contractions and factors that are able to modulate them, as well as the consequent afferent nerve activity, may be targets for drugs meant for treatment of OAB/DO. Neurourol.

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confidence: 99%

“…In humans, PGE 2 administration into the urinary bladder caused a strong sensation of urgency (27). It was speculated that PGE 2 reduced bladder capacity and increased bladder instability (27). Other studies have indicated that PGE 2 affects bladder smooth muscle directly, and activates capsaicin-sensitive bladder afferent (18,19).…”

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confidence: 99%

Prostaglandin facilitates afferent nerve activity via EP1 receptors during urinary bladder inflammation in rats

et al. 2006

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We examined the effects of loxoprofen, a cyclooxygenase inhibitor, and ONO-8711, an EP 1 -receptor antagonist, on afferent nerve activity during acetic acid (AA, 0.1% v/v)-induced inflammation of the rat urinary bladder. Distension stimulation was performed (vesical pressure of 30 cm H 2 O) for 2 min. The neuronal discharge was recorded from L6 dorsal root filaments. The discharge was observed just after the beginning of distension and increased gradually thereafter. When the vesical pressure returned to control value, the discharge diminished abruptly. AA infusion increased the total number of spikes to 198 ± 38.8% of control values. AA infusion also produced asynchronous discharge in 39% of the animals. Loxoprofen administration (1 mg/kg, i.v.) reduced the number of spikes to 40.3 ± 14.8% of control values. ONO-8711 administration (1 and 3 mg/kg, i.v.) reduced the number of spikes to 81.6 ± 1.6% and 32.2 ± 7.4% of control values, respectively. These data indicate that loxoprofen or EP 1 -receptor antagonist inhibit the inflammation-related neuronal activity. EP 1 receptors in the peripheral afferent nerve terminal and/or urothelium may facilitate the primary afferent nerve activity, which elicits the inflammation-induced micturition reflex.

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Comparison of the mode of action of prostaglandin E2 (PGE2) and sulprostone, a PGE2-derivative, on the lower urinary tract in healthy women

Cited by 71 publications

References 15 publications

Evaluation of Prostaglandin E2 and E-Series Prostaglandin Receptor in Patients with Interstitial Cystitis

Evaluation of Prostaglandin E2 and E-Series Prostaglandin Receptor in Patients with Interstitial Cystitis

Detrusor myocyte activity and afferent signaling

Prostaglandin facilitates afferent nerve activity via EP1 receptors during urinary bladder inflammation in rats

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