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Effects of kinin B(1) and B(2) receptor antagonists on overactive urinary bladder syndrome induced by spinal cord injury in rats - Abstract

Background and purpose: The kinin B1 and B2receptors have been implicated in physiological and pathological conditions of the urinary bladder.

However, their role in overactive urinary bladder (OAB) syndrome following spinal cord injury (SCI) remains elusive.

Experimental approach: We investigated the role played by kinin B1 and B2receptors in OAB after SCI in rats.

Key results: SCI was associated with a marked inflammatory response and functional changes in the urinary bladder. The SCI resulted in the B1 R mRNA up-regulation in the urinary bladder, dorsal root ganglion and spinal cord, as well as in B1 protein in the urinary bladder and B1 R and B2 R protein in the spinal cord. Interestingly, both B1 and B2 protein expression were similarly distributed in detrusor muscle and urothelium of SCI animals. In vitro stimulation of urinary bladder with the selective B1 or B2 agonist elicited a higher concentration-response curve in the SCI urinary bladder versus naive or sham urinary bladder. Cystometry studies revealed that the treatment of SCI animals with the B2 selective antagonist Icatibant reduced the amplitude and number of non-voiding contractions (NVCs). The B1 antagonist des-Arg9 -[Leu8 ]-bradykinin reduced the number of NVCs while the non-peptide B1antagonist SSR240612 reduced the number of NVCs, the urinary bladder capacity and increased the voiding efficiency and voided volume.

Conclusions and Implications: Taken together, these data showed the important roles of B1 and B2 receptors in OAB following SCI in rats and suggest that the blockade of these receptors could be potential therapeutic target for controlling OAB.

Written by:
Forner S, Andrade EL, Martini AC, Bento AF, Medeiros R, Koepp J, Calixto JB.   Are you the author?
Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, 88049-900, Florianópolis, SC, Brazil.

Reference: Br J Pharmacol. 2012 Aug 3. Epub ahead of print.
doi: 10.1111/j.1476-5381.2012.02127.x


PubMed Abstract
PMID: 22862305

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