Open AccessEndothelin-1 and Urinary Bladder Hyperplasia Following Partial Bladder Outlet Obstruction
Author(s) -
Masood Khan,
Nileema Shukla,
CS Thompson,
Faiz Mumtaz,
Dimitri P. Mikhailidis,
Robert J. Morgan
Publication year - 2000
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-200036051-00077
Subject(s) - bladder outlet obstruction , hyperplasia , urology , urinary bladder , medicine , muscle hypertrophy , neck of urinary bladder , endothelin 1 , endothelin receptor , detrusor muscle , antagonist , endocrinology , receptor , prostate , cancer
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 (ET(A) and ET(B))] in bladder vascular smooth muscle cells (SMC) proliferation. In the presence of 3-week-old BOO serum, ET(A) and ET(B) 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 ET(A) and ET(B) antagonists, respectively) and bladder neck (p = 0.01 for both ET(A) and ET(B) antagonists). These results suggest that ET-1 antagonists may prevent SMC hyperplasia associated with partial BOO.