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Keywords:

  • α1D-adrenoceptor;
  • β-adrenoceptor;
  • bladder outlet obstruction;
  • mRNA;
  • noradrenaline

Abstract

Aims

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).

Methods

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.

Results

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.

Conclusions

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.