PURPOSE: We examined the role of opioid receptors in the inhibition of bladder overactivity induced by electrical stimulation of the foot. MATERIALS AND METHODS: Experiments were done in 6 cats under α-chloralose anesthesia when the bladder was infused with saline or 0.25% acetic acid. Naloxone (1 mg/kg intravenously) was administered to block opioid receptors. To modulate reflex bladder activity electrical stimulation (5 Hz, 0.2 millisecond pulse width) was applied to the foot via skin surface electrodes at intensities of multiple times the threshold needed to induce observable toe movement. RESULTS: Acetic acid irritated the bladder, induced bladder overactivity and significantly decreased bladder capacity to a mean ± SE 25.3% ± 5.9% that of saline control capacity (p = 0.0001). Foot stimulation at 4T suppressed acetic acid induced bladder overactivity and significantly increased bladder capacity to 47.1% ± 5.9% of control (p = 0.0007). Naloxone did not significantly change bladder capacity during acetic acid irritation but it completely eliminated the inhibition of bladder overactivity induced by foot stimulation. CONCLUSIONS: Results indicate that opioid receptors have an important role in foot afferent inhibition of bladder overactivity. This raises the possibility that opioid receptors might be used as a pharmacological target to enhance the efficacy of foot stimulation for inhibiting bladder overactivity.
PURPOSE: We examined the role of opioid receptors in the inhibition of bladder overactivity induced by electrical stimulation of the foot. MATERIALS AND METHODS: Experiments were done in 6 cats under α-chloralose anesthesia when the bladder was infused with saline or 0.25% acetic acid. Naloxone (1 mg/kg intravenously) was administered to block opioid receptors. To modulate reflex bladder activity electrical stimulation (5 Hz, 0.2 millisecond pulse width) was applied to the foot via skin surface electrodes at intensities of multiple times the threshold needed to induce observable toe movement. RESULTS:Acetic acid irritated the bladder, induced bladder overactivity and significantly decreased bladder capacity to a mean ± SE 25.3% ± 5.9% that of saline control capacity (p = 0.0001). Foot stimulation at 4T suppressed acetic acid induced bladder overactivity and significantly increased bladder capacity to 47.1% ± 5.9% of control (p = 0.0007). Naloxone did not significantly change bladder capacity during acetic acid irritation but it completely eliminated the inhibition of bladder overactivity induced by foot stimulation. CONCLUSIONS: Results indicate that opioid receptors have an important role in foot afferent inhibition of bladder overactivity. This raises the possibility that opioid receptors might be used as a pharmacological target to enhance the efficacy of foot stimulation for inhibiting bladder overactivity.
Authors: Guoqing Chen; Jeffrey A Larson; P Dafe Ogagan; Bing Shen; Jicheng Wang; James R Roppolo; William C de Groat; Changfeng Tai Journal: J Urol Date: 2011-11-17 Impact factor: 7.450
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Authors: Abhijith D Mally; Yosuke Matsuta; Fan Zhang; Bing Shen; Jicheng Wang; James R Roppolo; William C de Groat; Changfeng Tai Journal: J Urol Date: 2012-09-25 Impact factor: 7.450
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Authors: Abhijith D Mally; Fan Zhang; Yosuke Matsuta; Bing Shen; Jicheng Wang; James R Roppolo; William C de Groat; Changfeng Tai Journal: J Urol Date: 2012-10-22 Impact factor: 7.450