Diabetic Urethropathy Compounds the Effects of Diabetic Cystopathy

Zhongguang Yang, Paul C. Dolber, Matthew O. Fraser

    Research output: Contribution to journalArticlepeer-review

    47 Scopus citations


    Purpose: The effects of short-term and long-term diabetes mellitus on urethral function were investigated to determine the contribution of urethral dysfunction to diabetes mellitus voiding dysfunction. Materials and Methods: Isovolumetric bladder pressure, urethral perfusion pressure and external urethral sphincter electromyography were measured in urethane anesthetized, female Sprague-Dawley rats (Charles River Laboratories, Wilmington, Massachusetts) 5 or 10 weeks after streptozotocin induced diabetes mellitus. Urethral responses to serial administration of the skeletal muscle blocker α-bungarotoxin, the nitric oxide synthase inhibitor Nω-nitro-L-arginine and the α-adrenergic agonist L-phenylephrine were determined in diabetes mellitus and age matched controls. Results: Peak bladder pressures and contraction amplitudes were significantly decreased in diabetes mellitus rats. Detrusor-sphincter dyssynergia occurred in approximately 30% of diabetes mellitus rats but never in controls. α-Bungarotoxin caused a greater decrease in baseline urethral perfusion pressure in diabetes mellitus rats than in controls (approximately 40% vs approximately 15%). Bladder contraction associated urethral smooth muscle relaxation amplitudes were significantly less in diabetes mellitus rats than in controls. Nω-nitro-L-arginine significantly suppressed urethral relaxation in controls but not in diabetes mellitus rats. L-phenylephrine significantly increased baseline urethral perfusion pressure in diabetes mellitus rats but not in controls. The unassociated conditions of insensitivity to N-nitro-L-arginine and hypersensitivity to L-phenylephrine were more common in 10-week diabetes mellitus rats than in control rats. Conclusions: Diabetes mellitus induced urethropathy is characterized by external urethral sphincter dysfunction, decreased urethral smooth muscle relaxation and nitric oxide responsiveness, and increased urethral smooth muscle responsiveness to α1-adrenergic agonists. These changes increase outlet resistance and, thereby, decrease voiding efficiency. This exacerbates voiding dysfunction, creating a vicious cycle of progressive lower urinary tract damage and dysfunction. Early intervention targeting outlet resistance may be indicated.

    Original languageEnglish (US)
    Pages (from-to)2213-2219
    Number of pages7
    JournalJournal of Urology
    Issue number5
    StatePublished - Nov 2007


    • adrenergic agonists
    • diabetes mellitus
    • nitric oxide
    • rats, Sprague-Dawley
    • urethra

    ASJC Scopus subject areas

    • Urology


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