Maintenance of bladder innervation in diabetes: A stereological study of streptozotocin-treated female rats

Langdale, Christopher L.; Thor, Karl B.; Marson, Lesley; Burgard, Edward C.

doi:10.1016/j.autneu.2014.06.007

Cited by 10 publications

(12 citation statements)

References 25 publications

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“…Immunohistochemical studies have demonstrated reduced bladder innervation and decreased cholinergic innervation in diabetes. In the present study, nerve‐evoked contractions of bladder strips were enhanced by 2 weeks of diabetes, consistent with previous functional studies .…”

Section: Discussionmentioning

confidence: 99%

Diabetes‐induced alterations in urothelium function: Enhanced ATP release and nerve‐evoked contractions in the streptozotocin rat bladder

Lee

Rose’Meyer

McDermott

et al. 2018

Clin Exp Pharma Physio

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Up to 80% of patients with diabetes mellitus develop lower urinary tract complications, most commonly diabetic bladder dysfunction (DBD). The aim of this study was to investigate the impact of diabetes on the function of the inner bladder lining (urothelium). Bladder compliance and intraluminal release of urothelial mediators, adenosine triphosphate (ATP) and acetylcholine (ACh) in response to distension were investigated in whole bladders isolated from 2- and 12-week streptozotocin (STZ)-diabetic rats. Intact and urothelium-denuded bladder strips were used to assess the influence of the urothelium on bladder contractility. Intraluminal ATP release was significantly enhanced at 2 weeks of diabetes, although not at 12 weeks. In contrast, intraluminal ACh release was unaltered by diabetes. Bladder compliance was also significantly enhanced at both 2 and 12 weeks of diabetes, with greatly reduced intravesical pressures in response to distension. Nerve-evoked contractions of bladder strips were significantly greater at 2 weeks of diabetes. When the urothelium was absent, nerve-evoked contractions were reduced, but contractions remained significantly elevated at lower frequencies of stimulation (<5 Hz) in diabetics. Interestingly, although relaxations of bladder strips to isoprenaline were unaltered by diabetes, removal of the urothelium unmasked significantly enhanced relaxations in strips from 2- and 12-week diabetic animals. In conclusion, diabetes alters urothelial function. Enhanced urothelial ATP release may be involved in the hypercontractility observed at early time points of diabetes. These alterations are time-dependent and may contribute to the mechanisms at play during the development of diabetic bladder dysfunction.

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Section: Discussionmentioning

confidence: 99%

Diabetes‐induced alterations in urothelium function: Enhanced ATP release and nerve‐evoked contractions in the streptozotocin rat bladder

Lee

Rose’Meyer

McDermott

et al. 2018

Clin Exp Pharma Physio

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“…The clinical DBD manifestations consist of storage and voiding problems, which substantially affect the quality of life[ 33 , 34 ]. Previous studies have shown that the pathogenesis of DBD was associated with the myogenic and neurogenic alterations of the bladder[ 11 , 16 , 35 , 36 ]. In our studies, we demonstrated that the contractile function of the bladder was damaged significantly in diabetic groups along with the morphological changes ( Fig 1 ).…”

Section: Discussionmentioning

confidence: 99%

Grape Seed Proanthocyanidin Extract Ameliorates Diabetic Bladder Dysfunction via the Activation of the Nrf2 Pathway

et al. 2015

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Diabetes Mellitus (DM)-induced bladder dysfunction is predominantly due to the long-term oxidative stress caused by hyperglycemia. Grape seed proanthocyanidin extract (GSPE) has been reported to possess a broad spectrum of pharmacological and therapeutic properties against oxidative stress. However, its protective effects against diabetic bladder dysfunction have not been clarified. This study focuses on the effects of GSPE on bladder dysfunction in diabetic rats induced by streptozotocin. After 8 weeks of GSPE administration, the bladder function of the diabetic rats was improved significantly, as indicated by both urodynamics analysis and histopathological manifestation. Moreover, the disordered activities of antioxidant enzymes (SOD and GSH-Px) and abnormal oxidative stress levels were partly reversed by treatment with GSPE. Furthermore, the level of apoptosis in the bladder caused by DM was decreased following the administration of GSPE according to the Terminal Deoxynucleotidyl Transferase (TdT)-mediated dUTP Nick-End Labeling (TUNEL) assay. Additionally, GSPE affected the expression of apoptosis-related proteins such as Bax, Bcl-2 and cleaved caspase-3. Furthermore, GSPE showed neuroprotective effects on the bladder of diabetic rats, as shown by the increased expression of nerve growth factor (NGF) and decreased expression of the precursor of nerve growth factor (proNGF). GSPE also activated nuclear erythroid2-related factor2 (Nrf2), which is a key antioxidative transcription factor, with the concomitant elevation of downstream hemeoxygenase-1 (HO-1). These findings suggested that GSPE could ameliorate diabetic bladder dysfunction and decrease the apoptosis of the bladder in diabetic rats, a finding that may be associated with its antioxidant activity and ability to activate the Nrf2 defense pathway.

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“…As the most important urologic complication of DM, diabetic cystopathy (DCP) has a prevalence ranging from 25% to 83%, [1][2][3][4] and is characterized by many urological dysfunctions including detrusor overactivity, diminished first sensation, elevated maximal cystometric capacity, impaired bladder compliance, and increased postvoid residual. 5 An accumulating body of evidence has indicated the possible pathogenesis of DCP is a multifactorial and profound process involved with the structural and functional impairments of DSM, [6][7][8][9][10][11] the diabeticinduced nerve damage, [12][13][14][15][16] and the secondary alterations of urothelium, [17][18][19] in which DSM could be considered the dominant target and the site of pathogenesis effect. Nevertheless, the exact mechanisms of DCP are still far from clear, and the promising prevention and treatments to this refractory disease remain to be explored.…”

Section: Introductionmentioning

confidence: 99%

Endoplasmic reticulum stress is involved in apoptosis of detrusor muscle in streptozocin‐induced diabetic rats

Wang

Yuan

et al. 2015

Neurourology and Urodynamics

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Maintenance of bladder innervation in diabetes: A stereological study of streptozotocin-treated female rats

Cited by 10 publications

References 25 publications

Diabetes‐induced alterations in urothelium function: Enhanced ATP release and nerve‐evoked contractions in the streptozotocin rat bladder

Diabetes‐induced alterations in urothelium function: Enhanced ATP release and nerve‐evoked contractions in the streptozotocin rat bladder

Grape Seed Proanthocyanidin Extract Ameliorates Diabetic Bladder Dysfunction via the Activation of the Nrf2 Pathway

Endoplasmic reticulum stress is involved in apoptosis of detrusor muscle in streptozocin‐induced diabetic rats

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