No conflict of interest reported by author(s).
Original Basic Science Article
Article first published online: 25 NOV 2008
Copyright © 2008 Wiley-Liss, Inc.
Neurourology and Urodynamics
Volume 28, Issue 4, pages 349–355, April 2009
How to Cite
Barendrecht, M. M., Frazier, E. P., Vrydag, W., Alewijnse, A. E., Peters, S. L.M. and Michel, M. C. (2009), The effect of bladder outlet obstruction on α1- and β-adrenoceptor expression and function. Neurourol. Urodyn., 28: 349–355. doi: 10.1002/nau.20642
Lori Birder led the review process.
- Issue published online: 6 APR 2009
- Article first published online: 25 NOV 2008
- Manuscript Accepted: 13 JUN 2008
- Manuscript Received: 31 MAR 2008
- bladder outlet obstruction;
To explore possible changes in expression and/or function of α1- and β-adrenoceptor subtypes as a cause for bladder dysfunction in a rat model of bladder outlet obstruction (BOO).
BOO was induced in rats by partial urethral ligature. Contraction and relaxation experiments were performed with isolated bladder strips from BOO, sham-operated and non-operated (control) rats 7 days after BOO induction. mRNA expression of α1- and β-adrenoceptor subtypes was assessed by quantitative real-time PCR.
Receptor-independent contraction or relaxation did not differ between BOO and sham rats. The α1-agonists methoxamine and A-61,603 caused only weak contraction without major differences between groups. Against KCl-induced tone, the β-adrenoceptor agonists noradrenaline and isoprenaline caused similar relaxation in BOO and sham rats, whereas relaxation in response to the β3-selective BRL 37,344 was attenuated. Against passive tension, noradrenaline induced relaxation in sham and control rats; in contrast, noradrenaline induced contraction at low concentrations and relaxation at high concentrations in BOO rats. The contraction component was abolished by the α1-antagonist prazosin. The mRNA expression of α1D-adrenoceptors was increased in BOO, whereas none of the other receptor mRNAs were up-regulated.
In a rat BOO model, weak contraction responses to α1-agonists and relaxation responses to β-agonists are not altered to a major extent. Nevertheless, relaxation responses to the endogenous agonist noradrenaline are turned into α1-adrenoceptor-mediated contraction responses in BOO, possibly due to an up-regulation of α1D-adrenoceptors. Neurourol. Urodynam. 28:349–355, 2009. © 2008 Wiley-Liss, Inc.