Urinary bladder hypertrophy and hyperplasia is a common feature of bladder outlet obstruction (BOO). The urinary bladder is known to synthesize endothelin-1 (ET-1). ET-1 is a potent vasoconstrictor peptide with mitogenic properties. Using an animal model of partial BOO we investigated the potential role of ET-1 and its receptor subtypes [endothelin-A and -B (ETA and ETB)] in bladder vascular smooth muscle cells (SMC) proliferation. In the presence of 3-week-old BOO serum, ETA and ETB antagonists significantly (p = 0.008) inhibited detrusor and bladder neck SMC proliferation. Cell counts were significantly reduced from the detrusor (p = 0.03, p = 0.01 with ETA and ETB antagonists, respectively) and bladder neck (p = 0.01 for both ETA and ETB antagonists). These results suggest that ET-1 antagonists may prevent SMC hyperplasia associated with partial BOO.
Departments of *Urology, and ‡Molecular Pathology & Clinical Biochemistry, Royal Free and University College Medical School (Royal Free campus), University College London, and †Department of Vascular Surgery, St Mary's Hospital, London, U.K.
Address correspondence and reprint requests to Dr Masood A. Khan, Research Registrar, Department of Urology, Royal Free Hospital, Pond Street, London NW3 2QG, U.K. E-mail:email@example.com
© 2000 Lippincott Williams & Wilkins, Inc.