Endothelin-1 and urinary bladder hyperplasia following partial bladder outlet obstruction

Urinary bladder hypertrophy and hyperplasia is a common feature of bladder outlet obstruction (BOO). The urinary bladder is known to synthesize endoth elin-1 (ET-1). ET-1 is a potent vasoconstrictor peptide with mitogenic prop erties. 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 presenc e of 3-week-old BOO serum, ETA and ETB antagonists significantly (p = 0.008 ) inhibited detrusor and bladder neck SMC proliferation. Cell counts were s ignificantly 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.