Abstract

Psychological stress can induce not only frequent urination but also exacerbation of bladder dysfunctions. However, the brain pathophysiological mechanisms underlying stress-induced effects on the micturition reflex are still unknown. Bombesin (BB)-related peptides and BB receptors in the brain have been reported to mediate and integrate stress responses. We have found that centrally administered BB induced frequent urination in rats through brain BB1 and BB2 receptors, serotoninergic nervous system/5-HT7 receptors and corticotropin-releasing factor (CRF) type1 (CRF1) receptors. Interestingly, the BB-induced frequent urination was independent of the BB-induced activation of the sympatho-adrenomedullary outflow, a representative response to stress. Because the outflow is well known to regulate micturition, the finding was very surprising. These findings indicate that brain BB1, BB2, 5-HT7 and CRF1 receptors could be new therapeutic targets for bladder dysfunction exacerbated by stress exposure.

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