Characterization of the capsaicin‐sensitive component of cyclophosphamide‐induced inflammation in the rat urinary bladder

Ahluwalia, Amrita; Maggi, Carlo Alberto; Santicioli, Paolo; Lecci, Alessandro; Giuliani, Sandro

doi:10.1111/j.1476-5381.1994.tb14845.x

Cited by 96 publications

(52 citation statements)

References 25 publications

(23 reference statements)

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“…Acrolein evokes the production of inflammatory mediators in the bladder (Ahluwalia et al, 1994), which induce Ca 2ϩ influx into primary sensory neurons (Linhart et al, 2003) and thus probably stimulate anandamide production in bladder afferents. However, increased anandamide concentration in the bladder could also be attributable to decreased anandamide hydrolysis by FAAH in bladder tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, Ca 2ϩ influx into capsaicin-sensitive primary sensory neurons, which occurs in inflammation (Linhart et al, 2003), results in the production of anandamide, the amount of which is comparable with that evoking TRPV1-mediated excitation of primary sensory neurons after PKA, PKC, and PLC activation in the cells (Premkumar and Ahern, 2000;Chuang et al, 2001;De Petrocellis et al, 2001;Ahluwalia et al, 2003a,b). Anandamide, through TRPV1, evokes action potential generation in capsaicin-sensitive primary afferents (Kollarik and Undem, 2004), which results in pain sensation (Schmelz et al, 2000) and release of neuropeptides, such as substance P, that are essential for the development of inflammatory hyperalgesia and hyperreflexia (Ahluwalia et al, 1994;Lecci et al, 1994a,b;Laird et al, 2000;Hunt and Mantyh, 2001).…”

Section: Introductionmentioning

confidence: 99%

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Anandamide-Evoked Activation of Vanilloid Receptor 1 Contributes to the Development of Bladder Hyperreflexia and Nociceptive Transmission to Spinal Dorsal Horn Neurons in Cystitis

Dinis¹,

Charrua²,

Avelino³

et al. 2004

J. Neurosci.

181

132

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The role of anandamide in the development of inflammatory hyperalgesia and visceral hyperreflexia was studied in the rat urinary bladder. Animals were given intraperitoneal cyclophosphamide injection, which evokes painful hemorrhagic cystitis accompanied by increased bladder reflex activity. These results suggest that anandamide, through activating TRPV1, contributes to the development of hyperreflexia and hyperalgesia during cystitis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Anandamide-Evoked Activation of Vanilloid Receptor 1 Contributes to the Development of Bladder Hyperreflexia and Nociceptive Transmission to Spinal Dorsal Horn Neurons in Cystitis

Dinis¹,

Charrua²,

Avelino³

et al. 2004

J. Neurosci.

181

132

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“…Dosage and route of administration of cyclophosphamide (CP) were determined from that described in literature. 15 …”

Section: Animalsmentioning

confidence: 99%

Protective effect of aminoguanidine against oxidative stress and bladder injury in cyclophosphamide‐induced hemorrhagic cystitis in rat

Abraham

Rabi

Selvakumar

2008

Cell Biochemistry & Function

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Cyclophosphamide (CP) is an antineoplastic agent that is used for the treatment of many neoplastic diseases. Hemorrhagic cystitis (HC) is a major dose limiting side effect of CP. Recent studies show that aminogaunidine, an inhibitor of inducible nitric oxide synthase is a potent antioxidant and prevents changes caused by oxidative stress such as depletion of antioxidant activity and tissue injury. The purpose of the study is to investigate the effect of aminoguanidine on parameters of oxidative stress, antioxidant enzymes and bladder injury caused by CP. Adult male rats were randomly divided into four groups. Control rats were administered saline; the AG control group received 200 mg/kg body wt of aminoguanidine; The CP group received a single injection of CP at the dose of 150 mg/kg body wt intraperitoneally. The CP þAG group received aminoguanidine (200 mg/kg body wt) intraperitoneally 1 h before the administration of CP. The rats were sacrificed 16 h after CP/saline administration. The bladder was used for light microscopic studies and biochemical studies. The markers of oxidative damage including protein carbonyl content, protein thiol, malondialdehyde and conjugated dienes were assayed in the homogenates along with the activities of the antioxidant enzymes, superoxide dismutase, glutathione peroxidase, catalase, and glutathione reductase and glutathione S transferase. In the bladders of CP treated rats edema of lamina propria with epithelial and sub-epithelial hemorrhage was seen. All the parameters of oxidative stress that were studied were significantly elevated in the bladders of CP treated rats. The activities of the antioxidant enzymes were significantly lowered in the bladders of CP treated rats. Aminoguanidine pretreatment prevented CP-induced oxidative stress, decrease in the activities of anti-oxidant enzymes and reduced bladder damage. The results of the present study suggest the antioxidant role for aminoguanidine in CP-induced bladder damage.

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“…sensory fibres [11] or systemic or intravesical instillation of SP causes increased vascular permeability and the Administration of an antagonist of the BK 2 receptor before intravesical instillation of cyclophosphamide or influx of leucocytes [1,12,13]. The release of histamine, leukotrienes and PGs by the bladder in response to SP xylene significantly reduced the subsequent inflammatory response [29][30][31]. Bradykinin exerts its inflammaor antigen sensitization and challenge suggests that these compound play an integral role in the pathogenesis tory eÂects at least in part via histamine release, increased cyclo-oxygenase-mediated production of proof bladder inflammation [1,4,14,15].…”

Section: Resultsmentioning

confidence: 99%

Kinetics of peptide‐induced release of inflammatory mediators by the urinary bladder

Saban

Bjorling

1997

British Journal of Urology

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Objective To investigate the release of inflammatory the release to below the spontaneous rates. All peptides, except CGRP and SOM, stimulated the release of mediators by the urinary bladder in response to exposure to pro-inflammatory peptides.PGE 2 between 0 and 30 min, and only VIP failed to stimulate the release of PGF 2a within 5 min of expoMaterials and methods Isolated guinea pig urinary bladder was incubated with 10 mmol/L each of substance sure. Substance P, NKA, VIP and BK stimulated the release of LTB 4 and this required >5 min of exposure. P (SP), neurokinin A (NKA), calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP),Conclusion These results indicate that the peptides evaluated induce an immediate and transient release octreotide acetate (a long-acting analogue of somatostatin, SOM), or bradykinin (BK), and the release of of histamine and activation of cyclooxygenase and delayed activation of 5-lipoxygenase. These actions histamine, prostaglandin (PG) E 2 , PGF 2a and leukotriene B 4 (LTB 4 ) was determined during 0-5, 5-30 and may directly regulate the participation of these peptides in the pathogenesis of cystitis. 30-120 min after addition. Results Substance P, NKA, VIP and BK stimulated the Keywords Bladder, neuropeptides, bradykinin, inflammation, octreotide release of histamine, while CGRP and SOM suppressed developed directed at this component of the inflammatory

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Characterization of the capsaicin‐sensitive component of cyclophosphamide‐induced inflammation in the rat urinary bladder

Abstract: Activation of CSPANs in the urinary bladder is likely to be due to the conversion of CYP into its active metabolite, acrolein, and not to a direct effect of CYP upon these nerve-endings.

Cited by 96 publications

References 25 publications

Anandamide-Evoked Activation of Vanilloid Receptor 1 Contributes to the Development of Bladder Hyperreflexia and Nociceptive Transmission to Spinal Dorsal Horn Neurons in Cystitis

Anandamide-Evoked Activation of Vanilloid Receptor 1 Contributes to the Development of Bladder Hyperreflexia and Nociceptive Transmission to Spinal Dorsal Horn Neurons in Cystitis

Protective effect of aminoguanidine against oxidative stress and bladder injury in cyclophosphamide‐induced hemorrhagic cystitis in rat

Kinetics of peptide‐induced release of inflammatory mediators by the urinary bladder

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