ArticleScientific reports2020
Pathophysiological changes of the lower urinary tract behind voiding dysfunction in streptozotocin-induced long-term diabetic rats.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Preclinical animal models of lower urinary tract dysfunction associated with metabolic syndrome.Nature reviews. Urology · 2026Review
- Robust noninvasive detection of hyperglycemia in mouse models of metabolic dysregulation using the novel Urination Index biomarker.Lab animal · 2025Article
- Time-dependent bladder activity changes in streptozotocin-induced female diabetic rats.Physiological reports · 2025Article
- Effect of moderate-intensity aerobic exercise on bladderNarra J · 2024Article
- A Brief Overview of Cholinergic and Phosphodiesterase-5 Inhibitors in Diabetic Bladder Dysfunction.International journal of molecular sciences · 2024Review
- Established and emerging treatments for diabetes-associated lower urinary tract dysfunction.Naunyn-Schmiedeberg's archives of pharmacology · 2022Review
- Potentilla chinensis aqueous extract attenuates cyclophosphamide-induced hemorrhagic cystitis in rat model.Scientific reports · 2022Article
- Effects of electroacupuncture on bladder dysfunction and the expression of PACAP38 in a diabetic rat model.Frontiers in physiology · 2022Article
- IR-61 Improves Voiding FunctionFrontiers in pharmacology · 2021Article
- Pathogenesis evidence from human and animal models of detrusor underactivity.Tzu chi medical journalReview
- Diabetic Cystopathy Occurs Independently from Other Atherosclerotic Risks.Case reports in neurologyArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We evaluated pathophysiological characteristics of the lower urinary tract dysfunction in a streptozotocin (STZ)-induced diabetic rat model. STZ (60 mg/kg) was injected intraperitoneally into male Wistar rats. In vitro bladder muscle strip experiments, in vivo cystometry, and simultaneous recordings of bladder pressure + urethral perfusion pressure (BP + UPP) with or without intravenous administration of L-arginine (300 mg/kg) or tadalafil (0.03 mg/kg) were performed at several time points. In vitro muscle strip experiments demonstrated that diabetic rats had significantly higher contractile responses to carbachol at 4-16 weeks, and a tendency for higher contractile responses to electrical field stimulation at 4-12 weeks, but this was reversed at 16 weeks. Diabetic rats had significant increases in voided volume, residual volume, bladder capacity, maximal voiding pressure, and amplitude and frequency of non-voiding contractions at 16 weeks. Tadalafil decreased the residual volume in diabetic rats. Diabetic rats had significantly higher UPP nadir and mean UPP during high-frequency oscillation at 16 weeks, which were reversed by tadalafil or L-arginine administration. The present results suggest that urethral relaxation failure, probably related to impairment of the NO/cGMP signalling pathway, rather than bladder contractile dysfunction may be a prominent cause for voiding dysfunction in STZ-induced chronic diabetic rats.
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