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Alpha1-adrenoceptor antagonists improve bladder storage function through reduction of afferent activity in rats with bladder outlet obstruction.

Authors: Yazaki, J  Aikawa, K  Shishido, K  Yanagida, T  Nomiya, M  Ishibashi, K  Haga, N  Yamaguchi, O 
Citation: Yazaki J, etal., Neurourol Urodyn. 2011 Mar;30(3):461-7. doi: 10.1002/nau.20984. Epub 2010 Sep 30.
Pubmed: (View Article at PubMed) PMID:20886573
DOI: Full-text: DOI:10.1002/nau.20984

AIMS: Using a rat BOO model, we determined whether alpha1-adrenoceptor (AR) antagonists (silodosin, prazosin) improve the bladder storage function by reducing afferent input from the lower urinary tract. MATERIALS AND METHODS: Male rats received partial bladder outlet obstruction or sham surgery were used. Four weeks following surgery, their voiding behavior was measured in a metabolic cage. BOO-rats were administered silodosin, prazosin or vehicle for 2 weeks subcutaneously using osmotic pump. At the post-drug condition, voiding behavior was measured again. The L6 spinal cord was removed and immunostained using anti c-Fos antibody. The rats were also performed continuous cystometry with saline without anesthesia or restraint at the pre- and post-drug conditions. RESULTS: Metabolic cage study showed the voiding behavior of BOO-rats was characterized by increase in frequency of urination and decrease in volume voided. Cystometric evaluation also showed the significant increase both in the number of successive voiding contraction and in contraction pressure. The administration of silodosin or prazosin significantly decreased urinary frequency and the number of micturition reflex but affected neither bladder contraction pressure nor residual volume. The number of c-Fos-positive cell significantly increased in BOO-rats, while significantly decreased in those receiving alphal-AR antagonists. CONCLUSIONS: The present study demonstrates that alpha1-AR antagonists silodosin and prazosin have an inhibitory effect on afferent input from the lower urinary tract independently of reducing urethral resistance, and thereby reduce the storage dysfunction secondary to BOO. This result suggests that alphal-AR, particularly alphalA-AR, may play an important role in the activation of the afferent pathway.

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CRRD Object Information
CRRD ID: 5688368
Created: 2012-02-29
Species: All species
Last Modified: 2012-02-29
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.