Prostanoids modulate reflex micturition by acting through capsaicin-sensitive afferents

Maggi, Carlo Alberto; Giuliani, Sandro; Conte, Bruno; Furio, Martino; Santicioli, Paolo; Meli, Paola; Gragnani, Lucia; Meli, Alberto

doi:10.1016/0014-2999(88)90221-x

Cited by 101 publications

(82 citation statements)

References 33 publications

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“…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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confidence: 99%

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

et al. 2006

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“…Many quantitative investigations have been carried out to develop a suitable model for physiopharmacological studies of micturition (1)(2)(3)(4)(5)(6)(7)(8). However, most of the studies have employed anesthetics and urethral catheter ization.…”

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Detrusor hyperreflexia induced by intravesical instillation of xylene in conscious rats.

et al. 1990

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Abstract-Intravesical instillation of xylene (30-50%) produced detrusor hyper reflexia characterized by a decrease in both the bladder capacity (time to micturition in the cystometrogram) and the urine volume in conscious rats placed in a restraining cage. At this time, the bladder tissue showed evidence of experimental cystitis with degradation of the epithelium and edema and hemorrhage in the submucosa, and a slight increase in the content of prostaglandin E2, which stimulates directly and/or indirectly capsaicin-sensitive sensory fibers. In addition, the bladder exhibited high amplitude spontaneous activity, but the bladder contractions induced by acetylcholine, substance P, prostaglandin E2 and capsaicin were not changed following intravesical instillation of xylene.In these hyperreflexic rats, atropine suppressed the amplitude of the micturition contraction and morphine increased the bladder capacity at similar doses as in sham-treated rats, while thiopental and indomethacin increased the bladder capacity at lower doses than in sham-treated rats. These findings indicated that intravesical instillation of xylene had produced detrusor hyperreflexia in conscious rats, and that the detrusor hyperreflexia is thought to be a useful model for evaluating the effect of a newly-developed agent on bladder function.

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“…In animals, intravesical administration of PGE 2 has been shown to provoke detrusor overactivity. It has been hypothesized that this is caused by activation of sensory bladder afferent neurons [6][7][8][9]. In addition, inhibition of EP1 and EP2 reduced the effect of PGE 2 dose-dependently in isolated guinea pig bladders [10].…”

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Ex vivo modulation of muscarinically induced contractions by PGE2 and an EP1 receptor antagonist in the guinea pig urinary bladder

Hohnen

Rahnama’i

Gink

et al. 2016

Bladder

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A B S T R A C T OBJECTIVE:Mechanical and physical stimuli can evoke release of several substances by the urothelium, for example, prostaglandin E2 (PGE 2 ), nitric oxide, acetylcholine and adenosine triphosphate. It has been shown, that PGE 2 and acetylcholine seem to act in a positive feedback on molecular level. This feedback was located in the urothelial/ suburothelial layer. Therefore, the aim of our study was to investigate the role of PGE 2 and one of its receptors, EP1, on muscarinic induced contractions. METHODS:The urethra and bladder of 24 male guinea pigs were dissected after sacrifice of the animal. The bladder was catheterized transurethrally and placed into a preheated organ bath filled with Krebs buffer. The bladders were repeatedly stimulated with the muscarinic agonist arecaidine alone or in combination with a) acetylsalicylic acid, b) PGE 2 or c) the EP1 antagonist ONO-8713. All drugs were applied at the serosal side of the bladder. Intravesical pressure was measured and amplitude and frequency of the arecaidine induced response were analyzed. RESULTS:Adding PGE 2 before muscarinic stimulations induced an amplifying effect on muscarinically induced contractions and inhibition of the PGE 2 producing enzymes prior to an arecaidine stimulation decreased the amplitude during the initial phase of the response. Inhibition of EP1 resulted in a decreased frequency during the second phase of the arecaidine response. CONCLUSIONS:In summary, this study provides evidence that the cholinergic and prostanoid systems in the urinary bladder act in a positive feedback loop and that the EP1 receptor plays a subtle role in this process.

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Prostanoids modulate reflex micturition by acting through capsaicin-sensitive afferents

Cited by 101 publications

References 33 publications

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

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

Detrusor hyperreflexia induced by intravesical instillation of xylene in conscious rats.

Ex vivo modulation of muscarinically induced contractions by PGE2 and an EP1 receptor antagonist in the guinea pig urinary bladder

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