Expression of bladder α₁-adrenoceptor subtype after relief of partial bladder outlet obstruction in a rat model

Abstract

Purpose: Many patients with benign prostatic hyperplasia require treatment for persistent storage symptoms, even when the obstruction is successfully relieved by surgery. Previous studies identified a characteristic increase in α 1D-adrenoceptor levels in the bladder in a bladder outlet obstruction (BOO) model. Here, we investigated the expression of α 1-adrenoceptor subtypes in the bladder after relief of partial BOO (pBOO) in a rat model. Materials and Methods: A total of 60 female Sprague-Dawley rats were randomly divided into three groups (sham-operated, pBOO, and pBOO relief groups), and the expression of α 1-adrenoceptor subtypes in the urothelium and detrusor muscle tissues was examined by western blot. Results: The expression of the α 1D-adrenoceptor was significantly higher in the urothelium and detrusor muscle tissue of the pBOO and pBOO relief groups than in the corresponding tissue of the sham-operated group. Additionally, the α 1A-adrenoceptor was predominant in the sham-operated group but significantly decreased in the urothelium in the pBOO group. No significant differences were found in α 1A-adrenoceptor levels in detrusor muscle or whole bladder. Conclusions: Our results showed that α 1D-adrenoceptor levels were consistently increased with pBOO, even after relief, suggesting that the α 1D-adrenoceptor might be a cause of persistent storage symptoms after relief of pBOO.

RETRACTED ARTICLE: Circular RNA Plasmacytoma Variant Translocation 1 (CircPVT1) knockdown ameliorates hypoxia-induced bladder fibrosis by regulating the miR-203/Suppressor of Cytokine Signaling 3 (SOCS3) signaling axis

“…This is one of limitations of the present study. In another aspect, BOO surgery used in this study caused bladder wall remodeling in rats, including hypertrophy and fibrosis, which is also the major characters of human BOO [ 50 ], meanwhile, this model has been applied in many similar reports [ 51 , 52 ]. We have demonstrated a role of circPVT1 on BOO development in animal model and cell-based model, but its application to human BOO were still obscure.…”

Characteristics of α1‐adrenoceptor antagonists‐induced ejaculatory dysfunction on spontaneous seminal emission in rats

“…Although we used normal rats, further study is needed to assess the effect of α 1 -AR antagonists on EjD in a rat model of BPH, as changes in α 1 -AR subtype expression in the urothelium have been shown in bladder outlet obstruction model rats. 35 In conclusion, the current results suggest that α 1 -AR antagonists inhibit SSE in normal rats and that the α 1A -AR blockade is closely involved with their inhibition. Furthermore, α 1 -AR antagonist-induced EjD could be a peripheral mechanism.…”

“…Although we used normal rats, further study is needed to assess the effect of α 1 ‐AR antagonists on EjD in a rat model of BPH, as changes in α 1 ‐AR subtype expression in the urothelium have been shown in bladder outlet obstruction model rats 35 …”

Molecular and Morphological Characteristics of the De-Obstructed Rat Urinary Bladder—An Update

“…Other examples are the increased α 1D receptor mRNA in the bladders and the normalization in the de-obstructed bladders. Others have found increased receptor protein in both groups [ 47 ]. This could perhaps be explained by the increase in cell membrane area per unit detrusor weight in the de-obstructed bladders caused by the shrinkage of the cells and by their corrugated surfaces.…”