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The effect of bladder outlet obstruction on alpha1- and beta-adrenoceptor expression and function
Maurits M Barendrecht1, Elfaridah P Frazier, Wim Vrydag
1Department of Pharmacology and Pharmacotherapy, Academic Medical Center, Amsterdam, The Netherlands.
Bladder outlet obstruction in rats alters noradrenaline responses, shifting them from relaxation to alpha(1)-adrenoceptor-mediated contraction. This may be linked to increased alpha(1D)-adrenoceptor expression.
Area of Science:
- Urology
- Pharmacology
- Physiology
Background:
- Bladder dysfunction is a common complication of bladder outlet obstruction (BOO).
- Adrenoceptor subtypes play a crucial role in bladder function.
- Changes in adrenoceptor expression or function may underlie BOO-induced bladder dysfunction.
Purpose of the Study:
- To investigate alterations in alpha(1)- and beta-adrenoceptor subtype expression and function in a rat model of BOO.
- To determine if these adrenoceptor changes contribute to bladder dysfunction.
Main Methods:
- Bladder outlet obstruction (BOO) was surgically induced in rats.
- Contraction and relaxation experiments were performed on isolated bladder strips.
- Quantitative real-time PCR was used to assess adrenoceptor mRNA expression.
Main Results:
- Relaxation responses to beta-adrenoceptor agonists were generally preserved, except for attenuation with BRL 37,344.
- Noradrenaline induced concentration-dependent contraction and relaxation in BOO rats, unlike control rats.
- Alpha(1D)-adrenoceptor mRNA expression was significantly increased in BOO rats.
Conclusions:
- While overall alpha(1)- and beta-adrenoceptor agonist responses are not drastically altered, noradrenaline's effect shifts in BOO.
- This shift involves alpha(1)-adrenoceptor-mediated contraction, potentially due to up-regulated alpha(1D)-adrenoceptors.
- These findings suggest a role for alpha(1D)-adrenoceptor changes in BOO-related bladder dysfunction.
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