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  • Title: Bladder angiotensin-II receptors: characterization and alteration in bladder outlet obstruction.
    Author: Yamada S, Takeuchi C, Oyunzul L, Ito Y.
    Journal: Eur Urol; 2009 Feb; 55(2):482-9. PubMed ID: 18378069.
    Abstract:
    BACKGROUND: It is assumed that angiotensin II (AngII) is significantly implicated in the pathogenesis of urinary dysfunction because of bladder outlet obstruction (BOO). OBJECTIVE: The current study was undertaken to characterize AngII receptors in the rat bladder in relation to BOO. MEASUREMENTS: Bladder AngII receptors were measured by a sensitive binding assay using a specific antagonist radioligand, [(125)I]-Sar(1)-Ile(8)-AngII, in bladder outlet-obstructed rats with and without repeated oral administration of telmisartan. RESULTS AND LIMITATIONS: [(125)I]-Sar(1)-Ile(8)-AngII bound specifically to the rat bladder homogenates with high affinity. This specific binding of [(125)I]-Sar(1)-Ile(8)-AngII was concentration-dependently displaced by the type 1 subtype (AT(1))-selective antagonists. These findings revealed the significant existence of pharmacologically relevant AngII (AT(1)) receptors in the bladder with relatively high density. Oral administration of telmisartan in rats has been shown to bind to the bladder AngII receptors. Bladder weight was about three times greater in bladder outlet-obstructed rats than in sham rats. Maximal number of binding sites (B(max)) for [(125)I]-Sar(1)-Ile(8)-AngII binding in the bladder was significantly (48%) decreased in the bladder-outlet rats when compared with sham rats, suggesting the down regulation of pharmacologically relevant AngII receptor sites. Notably, repeated oral administration of telmisartan (3mg/kg/d, 14 d) in rats completely prevented the development of a BOO-induced decrease in B(max) for bladder [(125)I]-Sar(1)-Ile(8)-AngII binding. Telmisartan treatment also effectively attenuated the increase in the bladder-wet weight caused by urinary outlet obstruction. CONCLUSIONS: Bladder AngII may be at least partly associated with the pathogenesis of urinary dysfunction occurring subsequent to BOO through stimulation of the AT(1) receptor subtype.
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