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Endothelin-1 and urinary bladder hyperplasia following partial bladder outlet obstruction
M A Khan1, N Shukla, C S Thompson
1Department of Urology, Royal Free and University College Medical School, University College London, UK. ktasmas@aol.com
Journal of Cardiovascular Pharmacology
|November 15, 2000
Summary
Endothelin-1 (ET-1) antagonists may prevent smooth muscle cell hyperplasia in bladder outlet obstruction (BOO). Blocking ET-1 receptors significantly reduced cell proliferation in a BOO animal model.
Area of Science:
- Urology
- Molecular Biology
- Physiology
Background:
- Urinary bladder hypertrophy and hyperplasia are common in bladder outlet obstruction (BOO).
- The urinary bladder synthesizes endothelin-1 (ET-1), a peptide with vasoconstrictor and mitogenic properties.
Purpose of the Study:
- To investigate the role of ET-1 and its receptor subtypes (endothelin-A and -B) in bladder smooth muscle cell (SMC) proliferation in a partial BOO animal model.
Main Methods:
- Utilized an animal model of partial BOO.
- Administered ET(A) and ET(B) antagonists in the presence of BOO serum.
- Assessed detrusor and bladder neck SMC proliferation via cell counts.
Main Results:
- ET(A) and ET(B) antagonists significantly inhibited detrusor and bladder neck SMC proliferation (p = 0.008).
- Cell counts were significantly reduced in the detrusor (p = 0.03, p = 0.01) and bladder neck (p = 0.01) with antagonist treatment.
Conclusions:
- ET-1 signaling through ET(A) and ET(B) receptors contributes to SMC hyperplasia in partial BOO.
- ET-1 antagonists show potential for preventing SMC hyperplasia associated with BOO.