Related Experiment Videos
Diabetes and diuretic-induced alterations in function of rat urinary bladder
E M Kudlacz1, A L Chun, K A Skau
1Division of Pharmacology, College of Pharmacy, Ohio State University, Columbus 43210.
Diabetes
|July 1, 1988
Summary
Diabetes causes bladder dysfunction due to increased urination and nerve damage. Studies show diabetic bladders have altered nerve control and reduced sympathetic function, distinct from diuretic effects alone.
Area of Science:
- Urology
- Endocrinology
- Neuroscience
Background:
- Diabetes mellitus is associated with bladder dysfunction.
- Distinguishing between diuretic effects and autonomic neuropathy is crucial for understanding these changes.
Purpose of the Study:
- To characterize bladder dysfunction in diabetes mellitus.
- To differentiate between changes caused by increased diuresis and autonomic neuropathy.
Main Methods:
- Comparison of four experimental conditions: control, streptozocin-induced diabetes, sucrose feeding (diuretic), and galactose feeding (diuretic).
- In vitro assessment of bladder compliance via intravesicular pressure measurements.
- In vivo examination of nervous system control through bladder infusion and monitoring contractions in anesthetized rats.
- Evaluation of sympathetic control using reserpine pretreatment.
Main Results:
- All treated groups showed increased urine output, bladder weight, protein, and DNA content.
- Diuresis led to increased bladder size and altered compliance properties.
- Diabetic bladders exhibited distinct nerve response patterns compared to diuretic models, suggesting diabetes-induced nerve regulation alterations.
- Diabetic bladders showed diminished sympathetic control, indicated by modest responses to reserpine.
Conclusions:
- Diuresis contributes to bladder enlargement and altered compliance.
- Diabetes mellitus induces specific alterations in bladder nerve regulation, distinct from diuretic effects.
- Diabetic bladder dysfunction involves a loss of sympathetic control, which may not be fully replicated by galactose-induced models.