Effects of NSAIDs on Bladder Function in Normal and Cystitis Rats: a Comparison Study of Aspirin, Indomethacin, and Ketoprofen

Takagi-Matsumoto, Hiroko; Ng, Betty; Tsukimi, Yasuhiro; Tajimi, Masaomi

doi:10.1254/jphs.fp0040098

Cited by 40 publications

(41 citation statements)

References 24 publications

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“…Aspirin, indomethacin or ketoprofen prolonged IC in the bladder infl ammation (22). The present study demonstrated that loxoprofen prolonged IC during the acetic acid infusion.…”

Section: Discussionsupporting

confidence: 60%

Loxoprofen inhibits facilitated micturition reflex induced by acetic acid urinary bladder infusion of the rats

2005

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Prostaglandins (PGs) are well known as one of the chemical mediators of infl ammation. Nonsteroidal anti-infl ammatory drugs (NSAIDs), PG synthesis inhibitors, are used for anti-nociception and/or anti-infl ammation. We examine the effect of loxoprofen, an NSAID, on micturiton in acetic acid-induced bladder infl ammation of the rats. In cystometrogram study with saline infusion into the urinary bladder, loxoprofen did not alter the interval of bladder contraction (IC, 107% of the control). IC was shortened by acetic acid infusion (65% of the control) and loxoprofen prolonged the IC (162% of acetic acid infused period). This prolonged IC was approximately same as the control. Loxoprofen did not alter the threshold pressure and the maximal voiding pressure. These data suggest that PGE 2 might not play a part of normal micturition and may play a part of the micturition refl ex during acetic acid infusion. That is, loxoprofen might be useful for pathological hyperrefl ex of the micturition.Urinary bladder controls two different physiological stages; storage of urine and micturition refl ex. Previous studies have mainly investigated the reflex pathway of the micturition (5, 25). In contrast, recent studies were interested in the storage mechanisms because over active bladder was commonly seen in elder people (2,8,21). During storage of the urine in the bladder, smooth muscles were stretched and it activated the afferent fi bers in the pelvic nerve (18). The activities were mediated through the sacral spinal cord and it stimulated the potine micturition center (6).When inflammation of the urinary bladder occurred, painful sensation was noticed and frequency of the micturition were increased (14). As indicated in many reports, infl ammation of the urinary bladder could excite the detrusor muscles with chemical mediators (17) and activate the afferent nerve terminals (1, 7).Prostagrandins (PGs) have been investigated for one of the chemical mediators of the infl ammation. In general, cyclooxgenase (COX) isoenzymes synthesize PGs from arachidonic acid at many organs including bladder smooth muscles and urothelium (4, 15). Indeed, PGE 2 in the urine was increased at the interstitial cystitis patients (11). Recent animal studies also demonstrated that COX-2 and PGE 2 were increased in cystitis rats (9, 24). Thus PGE 2 must be important for changing the micturition refl ex of the bladder infl ammation.Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for treatment of the infl ammation. Under anesthesia, NSAIDs increased the bladder capacity during the infl ammation in rats (23). It has been reported that anesthesia have infl uence to the micturition refl ex (26). So unanesthetized animals experiments must be performed. Hence we used

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“…Aspirin, indomethacin or ketoprofen prolonged IC in the bladder infl ammation (22). The present study demonstrated that loxoprofen prolonged IC during the acetic acid infusion.…”

Section: Discussionsupporting

confidence: 60%

Loxoprofen inhibits facilitated micturition reflex induced by acetic acid urinary bladder infusion of the rats

2005

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“…Tricyclic antidepressants, such as amitriptyline, may increase bladder capacity through β-adrenoceptors on the bladder and inhibition of the hypersensitivity of the bladder sensory nerves by blocking reuptake of noradrenalin and serotonin, as well as anticholinergic and antihistaminic effects (7,50,51). The anti-inflammatory effect of NSAIDs, such as indomethacin, helps to reduce the hypersensitivity of the bladder sensory nerves (52,53), although the anti-inflammatory effect on the bladder inflammation, which was indicated by increased bladder weight and induction of TNF-α mRNA expression, was not observed in the present administration schedule. A potent opioid analgesic, morphine, may be used for severe bladder pain and referred pain in IC patients (34), while it suppresses urinary frequency through spinal and supraspinal mechanisms by acting on μ-opioid receptors (54,55).…”

Section: Discussionmentioning

confidence: 99%

A Novel Mouse Model of Chronic Inflammatory and Overactive Bladder by a Single Intravesical Injection of Hydrogen Peroxide

et al. 2013

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“…Many published reports have proposed models of bladder inflammation (3,8,17,21,29,32). Acetic acid (AA) infusion into the urinary bladder of rats shortened inter-contraction interval (ICI) in cystometrograms (20,28).…”

mentioning

confidence: 99%

“…Cyclooxygenase synthesizes PGs from arachidonic acid, whereas non-steroidal anti-inflammatory drugs (NSAIDs) are known to inhibit cyclooxygenase. Because NSAIDs have been shown to prolong ICI, it is possible that they would inhibit afferent nerve activity during AA-induced inflammation (28,29). PGE 2 receptors are classified into four subtypes during the interval between distensions.…”

mentioning

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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Effects of NSAIDs on Bladder Function in Normal and Cystitis Rats: a Comparison Study of Aspirin, Indomethacin, and Ketoprofen

Cited by 40 publications

References 24 publications

Loxoprofen inhibits facilitated micturition reflex induced by acetic acid urinary bladder infusion of the rats

Loxoprofen inhibits facilitated micturition reflex induced by acetic acid urinary bladder infusion of the rats

A Novel Mouse Model of Chronic Inflammatory and Overactive Bladder by a Single Intravesical Injection of Hydrogen Peroxide

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

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