Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677481 (urinary frequency)
 1,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increase in bladder mucosal permeability can be reproduced by intravesical administration of protamine sulfate (PS); however, the influence of PS once administered into the bladder disappears within several days. We developed a chronic animal model of urothelial injury using PS. Insertion of a polyethylene catheter through the bladder dome was performed in female Wistar rats. The other end of the catheter was connected to an osmotic pump for continuous delivery of PS or vehicle for 2 wk. Urinary frequency (UF) and voided volume (VV) were measured in the metabolic cage. The fifth group of rats received a high dose of PS (10 mg/ml) for 2 wk and were followed for a further 2 wk without PS. The sixth group received a high dose of PS for 2 wk and loxoprofen (0.1 mg.kg(-1).day(-1)) for 4 wk. UF was increased, and VV was reduced in rats treated with a high dose of PS but not changed in rats treated with a vehicle or a low dose of PS (1 mg/ml). UF was further increased in the fifth group, while unchanged in the sixth group. Histological sections in rats treated with a high dose of PS demonstrated a loss of the upper layer of urothelial cells and an increased number of mast cells. PGE2 level in the bladder was significantly elevated in the fifth group. These results indicate that chronic urotherial injury leads to an increase in UF and a decrease in VV. Increased PGE2 level in the bladder is likely to be associated with long-lasting storage dysfunction.
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PMID:Long-lasting breaches in the bladder epithelium lead to storage dysfunction with increase in bladder PGE2 levels in the rat. 1855 Aug 66

The spontaneously diabetic Torii (SDT) rat has recently been established as a model of type 2 diabetes mellitus (DM). The usefulness of this rat model for the study of diabetic voiding dysfunction was investigated. Male SDT rats and male Sprague-Dawley (SD) rats were used. Voiding function was evaluated by a metabolic cage study and cystometry. Total voided volume for 24 h, mean voided volume, and urinary frequency for 24 h were significantly greater in SDT rats at the age of 36 weeks. From cystometry mean inter-micturition interval (IMI) was significantly longer in SDT rats at the age of 22 and 36 weeks. In SDT rats mean IMI was significantly longer at the age of 36 weeks than at the age of 22 weeks. Mean voiding pressure was significantly higher in SDT rats at the age of 22 and 36 weeks. In the present study, SDT rats showed typical diabetic voiding dysfunction similar to other diabetic rat models. It was suggested that activity of the bladder afferent pathways is decreased and the urethral relaxation mechanism is impaired in SDT rats. In addition, SDT rats are suitable to study chronic diabetic voiding dysfunction because they survive without insulin treatment for as long as 60 weeks.
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PMID:Long-term effects of diabetes mellitus on voiding function in a new model of type 2 diabetes mellitus, the Spontaneously Diabetic Torii (SDT) rat. 2005 41

We examined the inhibitory effects of loxoprofen, a cyclooxygenase inhibitor, and glycine, a major inhibitory neurotransmitter, on the micturition reflex in conscious rats and hypothesized that these drugs would interact synergistically to inhibit micturition. Voiding behaviors were assessed using a metabolic cage. Oral loxoprofen decreased the urinary frequency, and only a high dose(10 mg/kg) significantly reduced the voided volume. With cystometry, intravenous loxoprofen(0.1-3 mg/kg) and glycine (30 and 100 mg/kg) prolonged the intercontraction intervals (ICI) in adose-dependent manner, but did not change the maximum voiding pressure (MVP) in conscious rats. The combination of loxoprofen (3 mg/kg) and glycine (100 mg/kg) strongly prolonged the ICI more than with either drug alone. The lowest dose of loxoprofen (0.1 mg/kg) and glycine(30 mg/kg) did not affect either the ICI or the MVP, but their combination resulted in a significant increase in the ICI. These results suggest that the combined administration of loxoprofen and glycine produced a synergistic inhibitory effect on the micturition reflex.
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PMID:Synergistic effects of loxoprofen and glycine on the micturition reflex in conscious rats. 2457 98

Lower urinary tract symptoms (LUTS) including urinary frequency and nocturia are common in aging men. Recent studies have revealed a strong association of prostatic inflammation with LUTS. We developed an animal model of bacterial induced, isolated prostatic inflammation and examined the effect of prostatic inflammation on voiding behavior in adult C57BL/6J mice. Prostatic inflammation was induced by transurethral inoculation of uropathogenic E. coli-1677. Bacterial cystitis was prevented by continuous administration of nitrofurantoin. Hematoxylin and eosin (H&E) staining and bacterial culture were preformed to validate our animal model. Voiding behavior was examined by metabolic cage testing on post-instillation day 1 (PID 1), PID 4, PID 7 and PID 14 and both voiding frequency and volume per void were determined. Mice with prostatic inflammation showed significantly increased voiding frequency at PID 1, 7 and 14, and decreased volume per void at all time points, as compared to mice instilled with saline and receiving nitrofurantoin (NTF). Linked analysis of voiding frequency and voided volumes revealed an overwhelming preponderance of high frequency, low volume voiding in mice with prostatic inflammation. These observations suggest that prostatic inflammation may be causal for symptoms of urinary frequency and nocturia.
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PMID:Prostatic inflammation induces urinary frequency in adult mice. 2564 72

Psychological stress is associated with bladder dysfunction, however, the local bladder mechanisms affected are not well understood. This study aimed to determine how psychological stress, caused by social defeat or witness trauma, affects voiding behavior and bladder function. Pairs of male C57Bl/6J mice were placed in a custom-made plexiglass chamber with an aggressor ARC(S) mouse for 1 h/day for 10 days. The social defeat mouse was in physical contact with the aggressor, while the witness was physically separated but could observe interactions between its cage-mate and the aggressor. Age matched control pairs were used for comparison. Voiding analysis was conducted periodically over the 10 days. An ex vivo whole bladder preparation was used to assess functional changes after the period of stress. Plasma corticosterone levels were significantly increased by both social defeat and witness trauma stress when compared to unstressed controls. Voiding analysis revealed a significant decrease in voiding frequency in the social defeat group compared to control animals, indicating an altered voiding phenotype. Witness trauma did not alter voiding behavior. Bladder contractile responses to cholinergic stimulation were not significantly altered in either stress group, nor was relaxation to the beta-adrenoceptor agonist isoprenaline. However, nerve evoked contractile responses were significantly increased at all frequencies in bladders from social defeat but not witness trauma mice. Purinergic contractile responses were also significantly enhanced in this group. Social defeat also resulted in increased urothelial acetylcholine release during bladder distension, with no change in ATP release. In conclusion, functional bladder changes are dependent upon stressor type. Enhanced urothelial acetylcholine may desensitize bladder sensory nerves, which, coupled with more efficient voiding contractions due to enhanced nerve-mediated and purinergic detrusor responses, may account for the altered voiding phenotype observed. This study reports a male model of social defeat stress with reduced urinary frequency, with no voiding changes observed in the witness.
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PMID:Voiding Behavior and Efferent Bladder Function Altered in Mice Following Social Defeat but Not Witness Trauma. 3226 38