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Calcium channel antagonists prevent urinary bladder growth and neuroplasticity following mechanical stress

W D Steers1, M Albo, J B Tuttle

  • 1Department of Urology, University of Virginia, Charlottesville 22908.

The American Journal of Physiology
|January 1, 1994
PubMed

Insights

Calcium channel blockers like verapamil and diltiazem inhibit bladder and nerve growth in rats with urethral obstruction. These drugs reduced smooth muscle hypertrophy and nerve growth factor, suggesting calcium

Area of Science:

  • Urology
  • Neuroscience
  • Pharmacology

Background:

  • Cytosolic calcium (Ca2+) is hypothesized to regulate smooth muscle hypertrophy and growth factor production.
  • Urethral obstruction in rats leads to bladder and neuronal growth.

Purpose of the Study:

  • To investigate the role of Ca2+ channels in regulating bladder and neuronal hypertrophy in response to urethral obstruction.
  • To determine the effect of Ca2+ channel antagonists on nerve growth factor (NGF) levels in obstructed bladders.

Main Methods:

  • Administration of Ca2+ channel antagonists (verapamil, diltiazem) and an alpha 1-adrenergic antagonist (prazosin) to rats with surgically induced urethral obstruction.
  • Measurement of bladder weight, protein, and DNA content.
  • Retrograde neuronal labeling with Fluoro-Gold to assess neuronal size.
  • Quantification of nerve growth factor (NGF) in bladder tissue.

Main Results:

  • Verapamil and diltiazem prevented 30-45% of the increase in bladder weight, protein, and DNA content in obstructed rats.
  • These Ca2+ channel blockers reduced neuronal area profiles by 15-27% in major pelvic and dorsal root ganglia.
  • Bladders from obstructed rats treated with verapamil or diltiazem showed significantly lower NGF levels compared to untreated obstructed rats.
  • Prazosin decreased voiding frequency but did not impact bladder weight or neuronal size.

Conclusions:

  • Ca2+ channel antagonists effectively inhibit bladder smooth muscle hypertrophy and neuronal growth associated with urethral obstruction in rats.
  • Reduced NGF levels in obstructed bladders treated with Ca2+ channel blockers may contribute to the observed inhibition of neuronal growth.
  • Altered calcium handling is implicated in the development of bladder hypertrophy and associated neuronal changes during obstruction.

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