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Effects of nitric oxide inhibitors in mice with bladder outlet obstruction
Marcy Lancia Pereira1, Carlos Arturo Levi D'ancona2, Julio Alejandro Rojas-Moscoso3
1Departamento de Cirurgia, Faculdade de Ciências Médicas - UNICAMP, Campinas, SP, Brasil.
Purpose:
To investigate the lower urinary tract changes in mice treated with L-NAME, a non-selective competitive inhibitor of nitric oxide synthase (NOS), or aminoguanidine, a competitive inhibitor of inducible nitric oxide synthase (iNOS), after 5 weeks of partial bladder outlet obstruction (BOO), in order to evaluate the role of constitutive and non-constitutive NOS in the pathogenesis of this experimental condition.
Materials And Methods:
C57BL6 male mice were partially obstructed and randomly allocated into 6 groups: Sham, Sham + L-NAME, Sham + aminoguanidine, BOO, BOO + L-NAME and BOO + aminoguanidine. After 5 weeks, bladder weight was obtained and cystometry and tissue bath contractile studies were performed.
Results:
BOO animals showed increase of non-voiding contractions (NVC) and bladder capacity, and also less contractile response to Carbachol and Electric Field Stimulation. Inhibition of NOS isoforms improved bladder capacity and compliance in BOO animals. L-NAME caused more NVC, prevented bladder weight gain and leaded to augmented contractile responses at muscarinic and electric stimulation. Aminoguanidine diminished NVC, but did not avoid bladder weight gain in BOO animals and did not improve contractile responses.
Conclusion:
It can be hypothesized that chronic inhibition of three NOS isoforms in BOO animals leaded to worsening of bladder function, while selective inhibition of iNOS did not improve responses, what suggests that, in BOO animals, alterations are related to constitutive NOS.
Insights
Inhibiting nitric oxide synthase (NOS) isoforms in mice with bladder outlet obstruction worsened bladder function. Constitutive NOS, not inducible NOS, appears central to these alterations.
Area of Science:
- Urology
- Physiology
- Pharmacology
Background:
- Partial bladder outlet obstruction (BOO) in mice leads to significant lower urinary tract changes.
- Nitric oxide synthase (NOS) plays a role in regulating bladder function, with both constitutive and inducible isoforms potentially involved.
Purpose of the Study:
- To investigate the role of constitutive and inducible nitric oxide synthase (iNOS) in the pathogenesis of experimental bladder outlet obstruction.
- To evaluate the effects of L-NAME (non-selective NOS inhibitor) and aminoguanidine (iNOS inhibitor) on bladder function after 5 weeks of partial bladder outlet obstruction.
Main Methods:
- C57BL6 male mice underwent partial bladder outlet obstruction (BOO) or sham surgery.
- Mice were treated with either L-NAME or aminoguanidine, or vehicle, for 5 weeks.
- Bladder weight, cystometry, and tissue bath contractile studies were performed.
Main Results:
- BOO mice exhibited increased non-voiding contractions (NVC), larger bladder capacity, and reduced contractile responses.
- L-NAME treatment in BOO mice exacerbated NVC, prevented bladder weight gain, and enhanced contractile responses.
- Aminoguanidine treatment in BOO mice reduced NVC but did not prevent bladder weight gain or improve contractile responses.
Conclusions:
- Chronic inhibition of all NOS isoforms worsened bladder function in BOO mice.
- Selective inhibition of iNOS did not improve bladder function in BOO mice.
- These findings suggest that alterations in BOO are primarily related to constitutive NOS activity.
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