2003
DOI: 10.1007/s00210-003-0710-y
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The effect of inflammation on rat urinary bladder-dependent relaxation in coaxial bioassay system

Abstract: The effect of urinary bladder inflammation on the activity of a bladder-derived relaxant factor in the coaxial bioassay system was examined. Bladder inflammation was induced by intraperitoneal (i.p.) cyclophosphamide or intravesical lipopolysaccharide (LPS) injection to male rats. In precontracted rat anococcygeus muscle that was placed within rat bladder (coaxial bioassay system), acetylcholine induced a relaxation response, which was not altered by the denudation of urothelium or incubation with indomethacin… Show more

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Cited by 15 publications
(7 citation statements)
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“…The effect was interpreted as being caused by an unidentified relaxant factor released from bladder tissue (Fovaeus et al, 1999). The presence of a relaxant factor, released from the rat bladder by acetylcholine, was confirmed by Inci et al (2003), who also showed that bladder inflammation did not alter the synthesis and/or release of this bladder-derived relaxant factor. Hawthorn et al (2000) reported the presence of a diffusable, urothelium-derived inhibitory factor in the pig bladder, which could not be identified, but did not appear to be NO, a COX product, a catecholamine, adenosine, GABA, or an endothelium-derived relaxing factor sensitive to apamin.…”
Section: Peripheral Targetsmentioning
confidence: 86%
“…The effect was interpreted as being caused by an unidentified relaxant factor released from bladder tissue (Fovaeus et al, 1999). The presence of a relaxant factor, released from the rat bladder by acetylcholine, was confirmed by Inci et al (2003), who also showed that bladder inflammation did not alter the synthesis and/or release of this bladder-derived relaxant factor. Hawthorn et al (2000) reported the presence of a diffusable, urothelium-derived inhibitory factor in the pig bladder, which could not be identified, but did not appear to be NO, a COX product, a catecholamine, adenosine, GABA, or an endothelium-derived relaxing factor sensitive to apamin.…”
Section: Peripheral Targetsmentioning
confidence: 86%
“…Gross histological changes manifested as severe inflammation and focal erosions of the bladder resulting from the urothelial cytotoxicity may therefore be associated with a corresponding loss in the bladder contractility (over 50%). CYCL-induced bladder cystitis, therefore, appears to be a result of reactive oxygen species (ROS) overload or NO induction in the system36,37 triggering a cascade of events beginning with the membrane damage.…”
Section: Discussionmentioning
confidence: 99%
“…Inci et al 31 have examined the effect of inflammation on rat urinary bladder-derived relaxant factor in the coaxial bioassay system. The authors concluded that CP-induced bladder inflammation did not alter the synthesis and/or release of the bladder-derived relaxing factor, which is neither a cyclo-oxygenase product nor NO, but the altered contractility may be due to inflammation-induced oedema.…”
Section: Stated Thatmentioning
confidence: 99%