Sensory mechanisms of obstruction-induced detrusor overactivity

      Several hypotheses have been put forward to explain the mechanisms of detrusor overactivity, each of which either directly or indirectly implicates increased sensory signaling from the bladder. The aim of the study was to determine sensory neuron contribution to bladder overactivity. We used a model of gradually-developing bladder outlet obstruction in male guinea pigs to produce detrusor overactivity. Conscious voiding in metabolic cages, micturition contractions in urethane-anaesthetized guinea pigs, and contractile activity of whole isolated bladders in vitro were recorded in sham-operated and obstructed groups. Single unit extracellular recordings were made, in vitro, from pelvic afferent nerves in flat sheet bladder preparations. Obstructed guinea pigs showed a significant 3.8 times increase in conscious voiding frequency and a 4.4 times decrease in voiding volume (n = 18, P < 0.0001) compared to the sham-operated animals. In anaesthetized animals, the interval between micturition contractions during continuous cystometry did not differ between two groups, while the frequency and amplitude of non-voiding contractions was significantly increased in obstructed animals. Changes in conscious voiding in the obstructed animals was significantly associated with alterations in structural and functional contractile parameters of their isolated bladders. Stretch-induced firing of low threshold bladder afferents was reduced in obstructed bladders due to reduced bladder compliance. Using the spike-following frequency method, no increase in excitability of low threshold stretch-sensitive afferents was found in obstructed bladders. The data indicates that increased signaling from the bladders in obstructed guinea pigs is transmitted by low threshold stretch-sensitive afferents responding to increased localized contractile non-voiding activity of obstructed bladders.
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